# Brain Expert: Why Dementia Is Australia's Number One Killer

An episode of [Project 100 with Mark Bouris](https://invisiblenetwork.ai/podcast/1767053714), 24 May 2026, 1 h 25 min.

Audio: https://p.podderapp.com/2544644999/traffic.omny.fm/d/clips/2fb3740d-3436-44af-8cc0-a91900716aa5/05ac4e52-79fb-46b8-849c-b305000bd6d0/8059a5a2-379b-4fb1-a638-b45200826d7c/audio.mp3?utm_source=Podcast&in_playlist=ef13e652-7a19-41fd-9d0f-b305000bd6dc

All content and media by Project 100 is created and published online for informational purposes only. It is not intended to be a substitute for professional medical advice and should not be relied on as health or personal advice. **** Professor Matthew Kiernan is CEO of Neura and one of the nation's leading neurologists tackling the growing dementia crisis. Kiernan explores why dementia is now Australia's number one cause of death, the modifiable risk factors that could prevent 45% of cases, and the groundbreaking monoclonal antibody treatments now available for Alzheimer's disease. Kiernan explains how the Western Pacific region carries 60% of the world's dementia burden and why researchers are racing to develop blood biomarkers that could detect brain diseases decades before symptoms appear. We also get into: • Why dementia has overtaken heart disease as Australia's leading killer • The role of vascular health in brain function and cognitive decline • Blood biomarkers coming within five years for early detection • Monoclonal antibody treatments for Alzheimer's now available in Australia • The connection between contact sports, head injuries and neurodegeneration • How GLP-1 medications are showing promise for brain health • Sleep's critical role in clearing toxic proteins from the brain Join my exclusive Mentored+ community: https://mentored.com.au/become-a-member/ Subscribe to the Mentored newsletter here: https://mentored.com.au/newsletter See omnystudio.com/listener for privacy information.

## Transcript

[0:00] Speaker 1: Professor Matthew kindon Welcome to Project one hundred again made
[0:02] Speaker 1: and we probably run this on straight Talk as well,
[0:05] Speaker 1: if you don't mind, because I think there's a lot
[0:07] Speaker 1: of people who are in the straight talk audience who'd
[0:09] Speaker 1: like to hear what Project one hundred has got to
[0:11] Speaker 1: say about this, So appreciate your time.
[0:13] Speaker 2: No, thanks very much, Mark, and I really appreciate what
[0:15] Speaker 2: you're doing for the community to raise awareness of brain health.
[0:18] Speaker 1: Mental health. It's a huge topic and I was shocked
[0:22] Speaker 1: when I became aware that the broad umbrella of dementia
[0:26] Speaker 1: today is the number one cause of death in Australia
[0:32] Speaker 1: and so therefore it's overtaken heart or coronary attacks or
[0:37] Speaker 1: heart attacks or yeah, heart failure. First question to you
[0:41] Speaker 1: is is that just simply a result of us living
[0:45] Speaker 1: longer and therefore if we got through cancer and heart
[0:49] Speaker 1: problems that eventually our brain's going to get us. Is
[0:52] Speaker 1: that just that reason or you seeing younger people getting
[0:56] Speaker 1: it now?
[0:58] Speaker 2: Well, I think it's a combination of both of those factors.
[1:01] Speaker 2: But really, you know, as a doctor, when I was
[1:04] Speaker 2: a junior doctor, cardiovascular health was the key focus and
[1:08] Speaker 2: you know there was bypass surgery and people having heart attacks,
[1:11] Speaker 2: and it was the number one and so understandably, you know,
[1:16] Speaker 2: politicians in the community put a focus on trying to
[1:20] Speaker 2: understand the condition and treat it. And I think that's
[1:23] Speaker 2: really the gold standard to understand that, you know, heart
[1:26] Speaker 2: heart health and heart disease. You have to look after
[1:29] Speaker 2: vascular health, stop smoking, understand the risk factors cholesterol, blood pressure,
[1:35] Speaker 2: blood sugar levels. And it was with that understanding and
[1:39] Speaker 2: then some therapies coming through, and I think, you know,
[1:42] Speaker 2: everyone would accept that the statin evolution has changed cardiovascular health.
[1:48] Speaker 2: And then our buyer marker so understanding that we can
[1:50] Speaker 2: treat against cholesterol, and gradually you started to see cardiovascular
[1:54] Speaker 2: deaths going down. In my fields. In neurology, stroke was
[1:59] Speaker 2: always going up every single year, higher and higher and higher.
[2:02] Speaker 2: And then eventually they did an epidemiological study and they
[2:05] Speaker 2: saw that stroke was dropping. And the neurologists didn't actually
[2:09] Speaker 2: believe it, like, how could this be the case? They
[2:10] Speaker 2: repeated the study and sure enough, stroke was actually dropping.
[2:14] Speaker 2: And it's because we've learned from the vascular health approaches
[2:18] Speaker 2: from cardiologists and heart physicians and the same thing has happened.
[2:23] Speaker 2: So while that's been happening. And then obviously all the
[2:25] Speaker 2: great advances in cancer because of molecular biology, understanding genetics,
[2:29] Speaker 2: the human the whole human genome, all of these things
[2:32] Speaker 2: that are getting well understood, and no one has really
[2:35] Speaker 2: focused on inverticomus dementia. And I suppose as a community,
[2:39] Speaker 2: we've often thought that it's an elderly people's condition and
[2:43] Speaker 2: we didn't really care about it. And you know, okay,
[2:46] Speaker 2: if we end up a bit demented in a nursing hame,
[2:49] Speaker 2: that's the cost of living. But really what's happened alarmingly
[2:53] Speaker 2: is it's really come to the fore and we're seeing
[2:55] Speaker 2: there's a huge amounts of dementia and neuroady generation. And
[3:00] Speaker 2: in fact, this geographical region, the Western Pacific, carries three fifths,
[3:04] Speaker 2: so sixty percent of the world burden. What Yeah, and
[3:08] Speaker 2: it's going to be a massive cost, you.
[3:10] Speaker 1: Know about the budget. What is that?
[3:12] Speaker 2: Well, I think it's it's an unusual sort of racial mix.
[3:15] Speaker 2: But we've got you know, obviously a lot of Asian populations.
[3:19] Speaker 2: We've got South Pacific islanders, Obviously we've got the Anglos
[3:22] Speaker 2: from Western Europe. But it's a huge population. Firstly, and
[3:27] Speaker 2: they're prone to vascular, particularly related neuro problems, dementia, vascular
[3:34] Speaker 2: dementia in particular. And also I suppose there's a lot
[3:37] Speaker 2: of underdeveloped regions. So if we think about our neighboring countries,
[3:42] Speaker 2: you know, we've been very lucky, and Australia is lucky,
[3:44] Speaker 2: and there's Japan in Korea, but then it's mixed with
[3:48] Speaker 2: you know, great poverty. Thailand, Myanmar, Burma, Thaile, you know,
[3:53] Speaker 2: Indonesia all had huge populations. So the focus globally is
[3:59] Speaker 2: to try and fix up the Western Pacific and then
[4:02] Speaker 2: take some of the learnings from the Western Pacific and
[4:04] Speaker 2: do refinements, particularly in Western Europe and North America. So
[4:08] Speaker 2: as a neurologist, obviously I'm a bit prejudiced. I'm glad
[4:11] Speaker 2: there's a focus on brain health because it's really going
[4:14] Speaker 2: to be an evolution. And in fact, the reason I
[4:16] Speaker 2: did get into neurology was, you know, George bush Seni,
[4:19] Speaker 2: you're saying that the nineties were the decade of the brain,
[4:22] Speaker 2: and the brain has been left behind a little bit,
[4:24] Speaker 2: and now we're starting to understand these conditions and we're
[4:28] Speaker 2: going to be like the cardiologists of the nineties. We're
[4:31] Speaker 2: going to understand risk factors, we're going to be titrading
[4:34] Speaker 2: blood bier markers, We've got effective therapies and it's going
[4:37] Speaker 2: to be totally transformational. The joke about neurologists were they're
[4:42] Speaker 2: really good at making a diagnosis, but they don't do
[4:45] Speaker 2: any treatment. To go to the neurologists to get your
[4:47] Speaker 2: diagnosis and prepare you will, that was that's the prejudice
[4:53] Speaker 2: against us, poor old neurologists. But dare I say it.
[4:56] Speaker 2: We're going to a therapeutic era and it's really exciting.
[5:00] Speaker 1: And part of that, of course, is in your role
[5:03] Speaker 1: as Sea of Newer any Ura at UNSW or across
[5:09] Speaker 1: the road from the English horse Stable studying whatever it is.
[5:15] Speaker 1: But now Newer is as I understand it as, or
[5:19] Speaker 1: re Call is a joint venture between USW and the
[5:22] Speaker 1: Prince Well' Hospital. Is that right?
[5:24] Speaker 2: Yeah, so the Southeastern Sydney Local Health District and that
[5:26] Speaker 2: includes Prince of Wales, Saint George and Sutherlands. So and
[5:31] Speaker 2: it's a new initiative, but it's pretty big. I mean,
[5:34] Speaker 2: you've got a big premises of being any premises are
[5:36] Speaker 2: huge or brand new. How many people've got in your
[5:39] Speaker 2: ANEW about five hundred and fifty researchers focusing on brain
[5:43] Speaker 2: health and mental health. It's amazing and encourage everyone to
[5:46] Speaker 2: come out and visit like you've done, and we're very
[5:49] Speaker 2: keen to have, you know, really greater community involvement and connection.
[5:53] Speaker 1: Is that the biggest undertaking in the country. Yeah, I
[5:57] Speaker 1: would say it is.
[5:58] Speaker 2: The other sort of big centers around Australia will be
[6:01] Speaker 2: the Flory in Melbourne, there's the Queensland Brain Institute in Brisbane,
[6:07] Speaker 2: and there's the Parent Institute in Perth, but I think
[6:10] Speaker 2: they're the biggest entities, so only.
[6:12] Speaker 1: The biggest one in Sydney there, yeah, yeah. And does
[6:16] Speaker 1: government support it.
[6:19] Speaker 2: Well, of course the government does support it. But times
[6:22] Speaker 2: are tough and I suppose neuro was established on grand
[6:27] Speaker 2: funding so National Health and Medical Research Council, so NHMRC
[6:31] Speaker 2: and AARC Australian Research Council have been very very successful
[6:35] Speaker 2: in grants.
[6:35] Speaker 1: Do you have to apply for those grants?
[6:37] Speaker 2: And at present now the success rate for grants is
[6:40] Speaker 2: about eight to ten percent and the funding has really
[6:44] Speaker 2: taken a battering and I was actually pleased in the
[6:47] Speaker 2: budget to see an extra five hundred and eight million
[6:50] Speaker 2: coming towards medical research. And that had been driven by
[6:52] Speaker 2: a campaign through medical research institutes, but also great advocates
[6:57] Speaker 2: like Monique Ryan who'd been pushing for or to try
[7:00] Speaker 2: and get the MRFF amount fully released. But now with
[7:04] Speaker 2: you know, lowering government grants support, researchers have to reach
[7:09] Speaker 2: out more to the community and what are the best
[7:11] Speaker 2: what are the most successful ways? Well, the most successful
[7:13] Speaker 2: way to fund your research program is have an industry partner.
[7:17] Speaker 2: An industry you know they need to make money. For example, well,
[7:21] Speaker 2: I need any any farmer company, right. So examples that
[7:25] Speaker 2: we're working with very closely include Roach Diagnostics based in Switzerland,
[7:30] Speaker 2: ELI Lily or Lily Farmer the United States. They're they're
[7:34] Speaker 2: they're key tever are key partners for us to drive
[7:38] Speaker 2: our research programs. But the beauty about having an industry
[7:42] Speaker 2: partner is you're more likely to have what we call
[7:44] Speaker 2: impact and translations. In other words, your discoveries are going
[7:47] Speaker 2: to make it out to the patient, to the clinic.
[7:50] Speaker 2: And that's why the health district and the university are
[7:52] Speaker 2: engaged because they want to see better health outcomes. So
[7:56] Speaker 2: you're much more likely to get that if you have
[7:58] Speaker 2: an industry partner. Now, the other key way that Newer
[8:02] Speaker 2: has been surviving has been the support of the community.
[8:04] Speaker 2: And we've been very lucky to have fantastic philanthropic support
[8:09] Speaker 2: and the individuals who funded whole programs and developments of
[8:13] Speaker 2: the building. Margaret Ainsworth is responsible for the main building
[8:18] Speaker 2: at Nearer. But I think we're starting to see that
[8:21] Speaker 2: the community is investing in research with the desire to
[8:25] Speaker 2: have better health outcomes, and it's really it's great to see.
[8:29] Speaker 1: So let's just you measure vascular dementia and maybe you
[8:33] Speaker 1: could explain what is vascular dementia.
[8:37] Speaker 2: So vascular relates to the blood vessels, and dementia generally
[8:41] Speaker 2: means problems with memory and cognition. And the brain is
[8:46] Speaker 2: made up of nerves neurons that have has lining on it,
[8:51] Speaker 2: and the lining of the myeline is supplied the lining,
[8:54] Speaker 2: which is called myelin, is built through cholesterol and apo
[8:57] Speaker 2: lipoproteins and all of those sort of biochemical processes. But
[9:03] Speaker 2: it needs a vascular supply, It needs a blood. It
[9:06] Speaker 2: needs a blood.
[9:07] Speaker 1: So maybe we're just just for audience. Those things that
[9:12] Speaker 1: you just mentioned, Yeah, they're all fats, they're all flippers.
[9:16] Speaker 1: Fat's produced by our liver, so we're producing that.
[9:20] Speaker 2: We're endogenously so inside our body, yes, we are producing it.
[9:24] Speaker 2: And I think the other thing to say is the
[9:26] Speaker 2: brain is a network, so all of the brain is working,
[9:30] Speaker 2: communicating with itself all the time. We used to think that,
[9:33] Speaker 2: you know, one part of the brain might be memory,
[9:35] Speaker 2: one part of the brain might be vision. But that
[9:38] Speaker 2: was because we studied neurology on the basis of a
[9:42] Speaker 2: deficit like a stroke or an injury. In fact, okay,
[9:45] Speaker 2: a lot of the neurology understanding came from major wars,
[9:49] Speaker 2: so particularly World War One, bullet wounds in the back
[9:51] Speaker 2: of the head, people to understand that's the cerebellum, and
[9:54] Speaker 2: so it was looking at deficits. And one of the
[9:56] Speaker 2: great neurologists is a go called Charles Miller Fisher, and
[9:59] Speaker 2: he's said, you learn neurology stroke by stroke. So you
[10:02] Speaker 2: see a patient with a stroke, you see what part
[10:04] Speaker 2: of the brain is affected, and then you see what
[10:06] Speaker 2: the manifestation is that and then that's your understanding. But
[10:10] Speaker 2: now we see the brain more as a network. So
[10:13] Speaker 2: all of these parts of the brain are communicating through
[10:16] Speaker 2: these nerve fibers, and when the blood supply is affected,
[10:21] Speaker 2: they start not working as well as they should, so
[10:23] Speaker 2: the speed of the signal getting through is less. Sometimes
[10:27] Speaker 2: they die, so little parts of little holes start developing
[10:30] Speaker 2: small strokes, microstrokes at a very molecular level, So you
[10:34] Speaker 2: wouldn't see it if you had the brain in front
[10:36] Speaker 2: of you, but you put it under a microscope, you'd
[10:38] Speaker 2: see it.
[10:39] Speaker 1: And you probably can't detect it either while someone's alive.
[10:43] Speaker 2: Unless there's a certain amount happening, like a volume. It's
[10:46] Speaker 2: a volume effect, So we start to see it with
[10:48] Speaker 2: their MARI scans, but by that stage it's more often
[10:51] Speaker 2: than not more severe. So right at the beginning, and
[10:55] Speaker 2: that's the trouble, we don't know when this begins, so
[10:57] Speaker 2: it could be beginning twenty or thirty years before the
[11:00] Speaker 2: patient manifests any symptoms.
[11:03] Speaker 1: And what causes this blood supply problem? Like in other words,
[11:09] Speaker 1: I presume what we talk about is a reduction of
[11:12] Speaker 1: the blood to blow reduction of blood.
[11:13] Speaker 2: Supply, and it's really been driven the understanding through vascular researchers,
[11:20] Speaker 2: so cardiovascular hell, so understanding that the wall of the
[11:23] Speaker 2: blood vessel gets thicker, the sort of the lumen or
[11:26] Speaker 2: the hole in the middle gets smaller, less blood gets
[11:28] Speaker 2: out there. Sometimes the vessel actually breaks apart a little bit,
[11:32] Speaker 2: a bit of ooze, and you know, blood and proteins
[11:35] Speaker 2: escape into the brain. That's the process, and if that happens,
[11:39] Speaker 2: you know in general areas. Interestingly, one of the sort
[11:42] Speaker 2: of the key problems that you see is people start
[11:47] Speaker 2: falling over and everyone thinks, oh, falls are normal. No,
[11:50] Speaker 2: if you have a fall, that's abnormal. I mean, obviously
[11:53] Speaker 2: you have a fall you're running and your chip on
[11:55] Speaker 2: a gutter, that's understore. But if you're walking around the
[11:58] Speaker 2: house and you fall over, you're on the street, you
[12:00] Speaker 2: fall over, that's abnormal. You legs give away, Yeah, your
[12:03] Speaker 2: legs give away, or your balance is affected and you
[12:05] Speaker 2: fall over. That's often the beginning of understanding that someone
[12:10] Speaker 2: may be suffering from a vascular brain process. So falls
[12:13] Speaker 2: are very much characteristically linked. The other thing is obviously
[12:17] Speaker 2: your cognition. So family members notice that maybe you're not
[12:21] Speaker 2: as sharp as you were. You seem to be forgetting
[12:23] Speaker 2: things you might be I mean, sometimes, for instance, you
[12:28] Speaker 2: might drive the car home and you know, hit the
[12:29] Speaker 2: side of the car and the garage. You might not
[12:31] Speaker 2: even mention you've done it. You know, another family member
[12:34] Speaker 2: notices that there's a dent in the car.
[12:35] Speaker 1: How did that happen? So it's the.
[12:39] Speaker 2: Behavior and the fine tuning of motor function or brain
[12:42] Speaker 2: function is being affected. And it's usually often the family members,
[12:47] Speaker 2: people in the house, children, partners who notice and they
[12:50] Speaker 2: try and encourage a medical review because.
[12:53] Speaker 1: I remember when I come saw you just getting a
[12:57] Speaker 1: check up, and you may be do some physical moments
[13:02] Speaker 1: like walking and standing on one foot, and then you
[13:06] Speaker 1: sent me off to get an older center or adoptler.
[13:09] Speaker 1: I think you caught it on my crodod arteries. So
[13:14] Speaker 1: why would someone when would a doctor tell someone to
[13:17] Speaker 1: get that? And why would someone get that? What were those?
[13:20] Speaker 1: And those especially those tests we want to see my
[13:23] Speaker 1: old school physician tests. I remember I used to get that.
[13:26] Speaker 1: My doctor when I was a kid used to do that,
[13:28] Speaker 1: but doctor since then stopped doing it. What are you
[13:30] Speaker 1: looking for when you do those very fundamental tests?
[13:34] Speaker 2: So it's about motor function. So we're seeing how someone walks,
[13:37] Speaker 2: we're seeing their gate, we're seeing their gate length, and
[13:40] Speaker 2: then part of that is what we call tandem walking.
[13:42] Speaker 2: So the police stole our tests. This is a neurology test,
[13:45] Speaker 2: but doing heel in front of the toe in a
[13:47] Speaker 2: straight line, and these are markers for things like vascular dementia.
[13:51] Speaker 2: Also getting someone to stand on the spot and close
[13:54] Speaker 2: their eyes because if they're having problems with no function
[13:57] Speaker 2: in their legs in particular, other senses start to take off,
[14:01] Speaker 2: so they're relying on their eyes. But for instance, at nighttime,
[14:04] Speaker 2: when they get up in the middle of the night,
[14:05] Speaker 2: they fall over.
[14:06] Speaker 1: Yeah, so that's a.
[14:07] Speaker 2: Way to try and look at that, and coordination testing
[14:11] Speaker 2: in a general sense. Reflexes are used for us to
[14:15] Speaker 2: try to determine the level of We use a word
[14:17] Speaker 2: called lesion. Where is the lesions we're trying to work
[14:19] Speaker 2: out where the abnormality is, and by tradition we see
[14:25] Speaker 2: two two. We divide the nervous system up into central,
[14:28] Speaker 2: which is the brain and the spinal cord we call
[14:30] Speaker 2: it upper mode in urine or there's the peripheral and
[14:32] Speaker 2: that's the nerve and muscles in the arms and the legs,
[14:36] Speaker 2: and reflexes tell us where to go. So in other words,
[14:40] Speaker 2: if I test someone and they've got very brisk reflexes
[14:42] Speaker 2: in a territory, so I just tap them or I
[14:44] Speaker 2: don't even need a tendon hammer. That's suggesting upper mode
[14:47] Speaker 2: in urine or central problems. If I test their reflexes
[14:50] Speaker 2: and they've got no reflexes in a region, that would
[14:53] Speaker 2: suggest that the nerve supply is damage. So that's a
[14:57] Speaker 2: peripheral abnormality. So we're trying to see is this is
[14:59] Speaker 2: sense problem like vascular dementia or is it a peripheral
[15:03] Speaker 2: problem like a diabetic neuropathy.
[15:05] Speaker 1: Right, So, and then they're crottied Doppler.
[15:10] Speaker 2: Yeah, So it really depends on what the patient's presenting with.
[15:15] Speaker 2: But let's say the presentation might be a partners thinks
[15:18] Speaker 2: that they're not thinking as well as they were, or
[15:21] Speaker 2: as a family history, and with family history we use
[15:24] Speaker 2: typically under the age of fifty, so someone has had
[15:27] Speaker 2: a family members had either a heart attack or stroke
[15:30] Speaker 2: under fifty that's significant and so as part of my assessment,
[15:33] Speaker 2: we do investigations and the Doppler study is an ultrasound
[15:37] Speaker 2: looking at the carotid and vertebraladies. They're the main blood
[15:40] Speaker 2: vessels that go to the brain, supplying from the heart
[15:43] Speaker 2: from the heart directly, and if they start to get
[15:48] Speaker 2: closed off slightly, that can be the app that can
[15:51] Speaker 2: be the cause of the presentation. It was not a
[15:54] Speaker 2: blood flo enough blood flowing up and we use again
[15:57] Speaker 2: about a seventy percent market, so it's less than seventy
[15:59] Speaker 2: percent and flow. That's significant, right, But now with Doppler,
[16:04] Speaker 2: with technology, we can actually trace that up. When we
[16:06] Speaker 2: can go and now look at the blood vessels, the
[16:09] Speaker 2: middle cerebral artery, posterior cerebral artery, which form a sort
[16:13] Speaker 2: of circle inside the brain called the circle of Willis.
[16:16] Speaker 2: So we can study that now through ultrasound, and again
[16:20] Speaker 2: we can get some marker about blood flow.
[16:23] Speaker 1: Right, And so what would cause those arteries to do this?
[16:29] Speaker 1: I mean, obviously smoking is an issue, but yeah, is
[16:32] Speaker 1: it just high cholesterol, high low density cholesterol.
[16:36] Speaker 2: All of those factors, But definitely smoking would have been
[16:39] Speaker 2: probably the most common cause. And I've seen that evolution
[16:42] Speaker 2: now Like in the nineties we were seeing a lot
[16:44] Speaker 2: of credit artery. We use the words stenosis. It's less
[16:47] Speaker 2: common now. People don't smoke as much as they used to,
[16:50] Speaker 2: Like it's rare that you see smokers. Now you've mentioned
[16:54] Speaker 2: then cholesterol, so understanding like LDL in particular more than
[16:58] Speaker 2: about four point five or more more than two but
[17:01] Speaker 2: the total cholesterol of more than four point five is
[17:04] Speaker 2: significant blood sugar levels and obviously you know your body
[17:09] Speaker 2: mass index.
[17:10] Speaker 1: What about the so called apo b apolipo bread and B,
[17:13] Speaker 1: I mean, which is their carrier? So of the cholesterol
[17:17] Speaker 1: most people don't realize cholesterol doesn't get anywhere unless you've
[17:20] Speaker 1: got something we need to piggyback. Absolutely, And so that's
[17:24] Speaker 1: a new thing. Is there's a new test.
[17:25] Speaker 2: Yes, yeah, it's it's a new test. Yeah, And apper
[17:29] Speaker 2: LiPo protein is one of it. Turns out there's lots
[17:32] Speaker 2: of different types. There's lots of different forms. You know one, two, three, four, five,
[17:36] Speaker 2: four is the critical one. But these apper lipoproteins help
[17:41] Speaker 2: other processes, other nutrients come in and out of cells.
[17:46] Speaker 2: But the issue about appo LiPo protein E four is
[17:50] Speaker 2: that it is involved in the removal of amyloid and plaques.
[17:56] Speaker 2: So if you have higher numbers or manifestations of the
[18:00] Speaker 2: breakdown of amyloid in the brain is not as good.
[18:05] Speaker 2: So that makes you more prone to Alzheimer's disease. So
[18:09] Speaker 2: amyloid and tower proteins in the brain that are linked
[18:12] Speaker 2: to a specific form of dementia Alzheimer's.
[18:15] Speaker 1: Disease which forget forget from us basically can't remember stuff. Absolutely, yeah,
[18:21] Speaker 1: and that happens in one part of the brain more
[18:24] Speaker 1: prevalent in that hippocampus or the thing is that was
[18:26] Speaker 1: that right?
[18:26] Speaker 2: That's the most common and that that's the sort of
[18:29] Speaker 2: the center of memory function in our human brain. But
[18:31] Speaker 2: it doesn't have to be there, like it could also
[18:33] Speaker 2: be some people start losing their visions. It could be
[18:36] Speaker 2: in the occipital region. It can be lots of different
[18:39] Speaker 2: parts of the brain. But the more common part, yes,
[18:42] Speaker 2: is memory.
[18:42] Speaker 1: And is it fair to say that I don't know
[18:46] Speaker 1: where I read this, but vision and hearing are quite
[18:51] Speaker 1: important as early markers for that potentially you might be
[18:55] Speaker 1: getting dimension, might becoming your way down the track. Yeah,
[18:59] Speaker 1: why is that? Well?
[19:01] Speaker 2: I think this is really great work that came out
[19:02] Speaker 2: from the Lancet Commission, and they discovered fourteen factors which
[19:07] Speaker 2: could be modified to either prevent or treat dementia, modify
[19:12] Speaker 2: or prevent and one of those is hearing. And I
[19:16] Speaker 2: think that you know, I have a colleague as a neurologist,
[19:19] Speaker 2: and he started developing hearing problems and he noticed that
[19:21] Speaker 2: when he went to dinner party, he didn't really want
[19:23] Speaker 2: to engage because he couldn't hear what was going on.
[19:25] Speaker 2: So people start retreating and that then promotes the brain
[19:30] Speaker 2: not to function as well as it, you know, normally.
[19:33] Speaker 1: Retreating from what's social intrational.
[19:35] Speaker 2: Engagement, and so social engagement is another critical factor that
[19:39] Speaker 2: was identified by the Lancet Commission. So the more that
[19:42] Speaker 2: you're engaged in you know, a profession, a work, a environment,
[19:47] Speaker 2: a community, a sports environment, a rugby league club, the
[19:51] Speaker 2: better off people go. And if you're isolated the brain,
[19:56] Speaker 2: the brain doesn't like isolation. So this is all these
[20:00] Speaker 2: are all modifiable risk factors, and then how could you
[20:03] Speaker 2: sort of cut off a few of them? Well, firstly
[20:05] Speaker 2: like if you like exercise, are you involved in a
[20:07] Speaker 2: in a community approach or as a particular exercise that
[20:10] Speaker 2: you like doing aerobic type of exercise, but also resistance training,
[20:14] Speaker 2: and these again are all modifiable risk factors for dementia.
[20:19] Speaker 2: Another part of that that's only really come out in
[20:21] Speaker 2: the last few years is an understanding what we're called frailty.
[20:24] Speaker 2: So you might have said, O, someone looks a bit frail.
[20:26] Speaker 2: That doesn't really mean anything, but frailty is it's a
[20:29] Speaker 2: two way process between the body and all of the
[20:32] Speaker 2: body organs and the brain. So when the brain stops working,
[20:36] Speaker 2: the organs don't work as well. But if the organs
[20:38] Speaker 2: don't work as well, the brain stops working as in converse.
[20:42] Speaker 1: So your dale's you'll get frail.
[20:45] Speaker 2: How can you prevent yourself from becoming frail? Well, resistance training,
[20:49] Speaker 2: high protein diets, aerobic training, stay engaged with the community.
[20:53] Speaker 2: These are the things that are going to help brain health.
[20:55] Speaker 1: I remember Mark Penny, Professor Mark Pennie M's showing about
[20:57] Speaker 1: because I was talking about him about his dad, Ron, Yeah,
[21:00] Speaker 1: who died from dementia, and Ron was like a genius
[21:04] Speaker 1: skinny fit walked up the stairs to a level of
[21:07] Speaker 1: whatever it was every day at Sir Vincent's. And I
[21:10] Speaker 1: said to Mark, are you worried about your genetic predisposition perhaps,
[21:17] Speaker 1: and would you bother getting a genetic test for dementia?
[21:20] Speaker 1: And he said no? And I said why? And he
[21:22] Speaker 1: said to me The reason why, he said, is because
[21:25] Speaker 1: even if I find out the solution right now, I
[21:28] Speaker 1: don't have any symptoms. But the solution right now would
[21:31] Speaker 1: be to do high intensity exercise, he said, So I'm
[21:35] Speaker 1: mols do it. Anyway, whether I get a diagnosis or not,
[21:38] Speaker 1: they're only the diagnosis because getting the diagnosis can cause
[21:41] Speaker 1: a lot of anxiety, and people do retract socially and
[21:44] Speaker 1: all sorts of things. He said, I'm better probably not knowing,
[21:48] Speaker 1: but doing the very thing that they would recommend me
[21:53] Speaker 1: do anyway. And so how does high intensity exercise assist
[21:59] Speaker 1: in that regard?
[22:01] Speaker 2: Well, I think obviously he was a visionary, but yeah,
[22:04] Speaker 2: when you exercise, for instance, blood vessels dilate, so the
[22:07] Speaker 2: blood vessels dilate, more blood flow starts going through brain,
[22:10] Speaker 2: in your brain and all over your body, but in
[22:12] Speaker 2: your muscles. So it's just reflecting what's going on. But
[22:16] Speaker 2: a number of conditions are also associated with other metabolic
[22:19] Speaker 2: changes in the brain and the body in a general sense,
[22:22] Speaker 2: so insulin resistance, metabolic health, mitochondrial function, so all the
[22:28] Speaker 2: cellular approaches, inflammation, inflammation in the brain, inflammation in the
[22:32] Speaker 2: organs of the body.
[22:33] Speaker 1: So all of.
[22:34] Speaker 2: These are improved through exercise and high intensity exercises. As
[22:39] Speaker 2: Matt Penny suggested back then, I think the other thing is,
[22:42] Speaker 2: and I understand what he's saying as well, there's a
[22:44] Speaker 2: stigma and people don't necessarily want to be associated with
[22:47] Speaker 2: any of these conditions. But I think what we've got
[22:50] Speaker 2: to is try and turn that around as a community
[22:52] Speaker 2: and say, well, we're focusing on brain health. We want
[22:55] Speaker 2: optimal brain function, and we want to get into it early,
[22:59] Speaker 2: and we want to maintain it throughout the course of
[23:01] Speaker 2: your life. So wouldn't it be great if people started
[23:04] Speaker 2: going to their general practitioners at the age of thirty
[23:06] Speaker 2: and had a brain health check to prevent dementia and
[23:11] Speaker 2: erodegeneration in their sixty seventies, eighties, nineties. We don't know
[23:15] Speaker 2: how long we're going to live for, but it's still
[23:17] Speaker 2: going upwards. So I think that we can try and
[23:20] Speaker 2: encourage a more healthy approach to brain health.
[23:24] Speaker 1: It was funny, you know, today, knowing I was going
[23:26] Speaker 1: to talk to you, I actually had an appointment, just
[23:28] Speaker 1: a general point with my GP, who's actually fantastic. I've
[23:33] Speaker 1: got to give him, I've got to get shower him
[23:34] Speaker 1: out now. And he's new. He's new, he's a young
[23:38] Speaker 1: guy I knew, and he and I have all sorts
[23:40] Speaker 1: of conversations similar to you and I about all sorts
[23:43] Speaker 1: of things. And I said to him, I wonder whether
[23:45] Speaker 1: or not I should have say, two days off from
[23:50] Speaker 1: exercise and go and get a blood test for BDNF
[23:53] Speaker 1: brain revenue tropic factor. And he said, oh, he said, okay,
[23:58] Speaker 1: there's not a bad idea, but he can't find any
[24:00] Speaker 1: where who does that. He's still searching. He hasn't texted yet,
[24:04] Speaker 1: but he's still searching. And the only reason I was
[24:06] Speaker 1: saying that was because you know, I'm with things. You know,
[24:10] Speaker 1: as you know, my mother passed away from a new
[24:12] Speaker 1: disease or als and I've got a dimension on the
[24:15] Speaker 1: other side, So you know, I get nervous about these things,
[24:17] Speaker 1: but not so much that I'm over nervous. I'm not paranoid,
[24:21] Speaker 1: but but I take the view I'm a contra good
[24:24] Speaker 1: or something about it. I got to talk to people,
[24:26] Speaker 1: that's what this whole show's about. And and I thought, well,
[24:30] Speaker 1: I as I understand it, that particular MOLECULEAR gets produced
[24:36] Speaker 1: in your brain when you exercise is very good for
[24:40] Speaker 1: brain health, but no one knows what the level is.
[24:44] Speaker 1: No one's actually asked me to do a test. And
[24:48] Speaker 1: I'm assuming he can find he can find someone can
[24:50] Speaker 1: do it. You probably know the incident anyway, But what
[24:52] Speaker 1: are some of the things that you think Australians or
[24:55] Speaker 1: people listening to this show should be asking their doctor
[24:59] Speaker 1: to get tested, even if it's just baselining you now
[25:02] Speaker 1: in a relation to brain health, are there things that
[25:04] Speaker 1: you should be asking apart from the obvious ones, and
[25:06] Speaker 1: the obvious ones of the heart was good you want, Tommy,
[25:10] Speaker 1: if it's good for your heart's good for your brain exactly. Yeah,
[25:12] Speaker 1: But apart from those, you know, ApoB little A E
[25:17] Speaker 1: and all that stuff. Apart from those ones, are there
[25:19] Speaker 1: any specific things you should be getting tested when you
[25:22] Speaker 1: ask for a blood test from your doctor relative to
[25:24] Speaker 1: your brain health.
[25:25] Speaker 2: Well, you've already articulated the main ones currently, but this
[25:29] Speaker 2: is a rapidly evolving landscape. So, for instance, at Neuroscience
[25:33] Speaker 2: Research Australia have formed a partnership with Roast Diagnostics platform
[25:37] Speaker 2: and part of the reason for that is to get
[25:39] Speaker 2: blood bio markers as a Medicare item number, so that
[25:43] Speaker 2: people can go to their GP and have all of these.
[25:46] Speaker 1: Get numb for free.
[25:46] Speaker 2: Yeah, and that's where it's going to be. That's going
[25:49] Speaker 2: to be in the next five to ten years, right,
[25:51] Speaker 2: And some of those markers are specifically, you know, identified
[25:57] Speaker 2: with particular conditions. But there are things called neurofilement, so
[26:00] Speaker 2: the neurofilament goes up in your blood when there's been
[26:04] Speaker 2: some nerve damage. There are other markers we call GFAPP.
[26:09] Speaker 2: These are blood tests that can suggest a particular diagnosis.
[26:17] Speaker 2: There's been a huge study in the UK and they've
[26:20] Speaker 2: taken blood and clinical examinations from fifty thousand people and
[26:25] Speaker 2: they've gone back to the blood bio markers and they're
[26:27] Speaker 2: show them that if five particular proteins in the blood
[26:30] Speaker 2: go up about ten years before Alzheimer's disease develops, and
[26:35] Speaker 2: that's where we're going to be going. So we're going
[26:37] Speaker 2: to be testing these in healthy individuals and then we
[26:40] Speaker 2: can start to treat against these blood bio markers to
[26:44] Speaker 2: try and maximize brain health. It's not here at the present,
[26:47] Speaker 2: but there's a lot of work going on in your
[26:49] Speaker 2: hurry right now.
[26:50] Speaker 1: I can't wait forever. Yeah no, because one of these
[26:54] Speaker 1: I want to ask you is can you test? Can
[26:56] Speaker 1: I do a blood test today for amyloids in tower?
[27:02] Speaker 2: At the moment you can't. But that's exactly so this
[27:05] Speaker 2: sort of diagnostic pathway is to bittering amyloid and tau
[27:08] Speaker 2: for Alzheimer's disease, TDP forty three for motor neurone disease,
[27:13] Speaker 2: in front of temperal dementia, alpha si nucleon for leuis
[27:16] Speaker 2: body dementia, Parkinson's disease. That's where it's going to be
[27:19] Speaker 2: and we're going to see what are those levels, but
[27:21] Speaker 2: we can't really at the moment. We haven't done large
[27:24] Speaker 2: population studies to know what that range should be.
[27:27] Speaker 1: It's just people. You don't have a range, So that's
[27:30] Speaker 1: cutting in. Yeah, So do you think in the next
[27:34] Speaker 1: five years these are some of these are realistically able
[27:38] Speaker 1: to be done?
[27:39] Speaker 2: I'd say with absolute guarantee they will be. And you'll
[27:42] Speaker 2: be going to the doctor with a blood result like
[27:44] Speaker 2: you do now with a full blood count hemoglobin and
[27:46] Speaker 2: they'll say, oh, your neurofilm and is slightly high. This
[27:49] Speaker 2: is the treatment to bring it down towards roughly normal
[27:52] Speaker 2: levels or that's really high. We need to do some
[27:55] Speaker 2: more investigations on that one. We need to lumber Puncher
[27:57] Speaker 2: and MRIs again. So I think it's going to start
[27:59] Speaker 2: to deter and the way forward. But then also linked
[28:03] Speaker 2: to that, we're going to start having treatments and we
[28:05] Speaker 2: have now two treatments for Alzheimer's, these monoclonal antibodies, and
[28:10] Speaker 2: there's a lot more on the horizon coming through, so
[28:12] Speaker 2: it's a very much a therapeutic era.
[28:15] Speaker 1: Well, so I do want to talk about those monoclone
[28:18] Speaker 1: antibody treatments in a moment, because I have one. As
[28:22] Speaker 1: you know, I text you. But I have one friend
[28:24] Speaker 1: of mine who's in his eighties, and I don't know
[28:27] Speaker 1: whether it's him or his wife showed him this thing
[28:29] Speaker 1: and he knows I have this show, and he sent
[28:32] Speaker 1: me the text, and I said, don't worry. I'm going
[28:34] Speaker 1: to get Matthew Kin and I'm going to ask him
[28:35] Speaker 1: the question because he actually is worried at his age
[28:39] Speaker 1: about dementia. I'm genuinely worried by the way he's in
[28:44] Speaker 1: great shape. But people do get nervous about the stuff, mate,
[28:47] Speaker 1: They get really anxious. I mean, I think there's more anxiety.
[28:51] Speaker 1: Of all the guys I know around my age. The
[28:54] Speaker 1: one thing that is, particularly the ones who played footy
[28:57] Speaker 1: or boxed or did anything like that. Had we're in
[29:00] Speaker 1: contact spoorts, they are all worried about dementia. It's like
[29:05] Speaker 1: it's a big deal. You'd be seeing as in your religis.
[29:08] Speaker 1: But it's a big deal.
[29:09] Speaker 2: Yeah, and I think again industry has taken that on
[29:12] Speaker 2: board as well. There was recently a superannuation conference and
[29:15] Speaker 2: all of the key superproviders. You know, imagine you've done
[29:19] Speaker 2: your whole life, you've worked, you set yourself up, and
[29:22] Speaker 2: then your cognition goes down. So it's it's incredibly important
[29:26] Speaker 2: and I can see why people are worried. I'm worried,
[29:29] Speaker 2: but we don't have a way to identify who is
[29:31] Speaker 2: at the greatest risk at the moment. And that's why
[29:35] Speaker 2: the focus on making brain health, you know, the key
[29:38] Speaker 2: treatment area for our community is critical and that's why
[29:43] Speaker 2: it's happening. Everyone's worried about it.
[29:45] Speaker 1: Well, government should be worried about too, because some mean
[29:48] Speaker 1: their job, is my view, their job is to increase
[29:51] Speaker 1: their standard of living. Our stand living. That the ultimate
[29:54] Speaker 1: it's about stand living. And there are lots of measurements
[29:56] Speaker 1: for that. One measurement that should be how long you
[29:58] Speaker 1: can live on this planet, how well you live during
[30:01] Speaker 1: that period. And living with dementia, like when it's full
[30:05] Speaker 1: blown at least, is not living, you know, like it's
[30:09] Speaker 1: pretty dreadful on everyone. Else around you, Like if you
[30:12] Speaker 1: someone said to me today, ail to you or anybody, Look,
[30:14] Speaker 1: you know, how would you see yourself when you're eighty
[30:16] Speaker 1: five or ninety. And by the way, medical technology you'll
[30:19] Speaker 1: get us there now because they can fix the hard thing,
[30:22] Speaker 1: and replace the hard thing, and fix the guineas and
[30:23] Speaker 1: fix just better really accept this thing. And if they said,
[30:29] Speaker 1: if you were to rate your standard living, one thing
[30:31] Speaker 1: is you probably don't want to be confronted with is
[30:35] Speaker 1: your kids having to bathe you and not be recognized
[30:40] Speaker 1: by you, or your kids have having to put you
[30:42] Speaker 1: in a nursing home because you turn a little bit
[30:44] Speaker 1: violent because you've got dementia. That would be probably the
[30:48] Speaker 1: lowest stand of living I can imagine for me. I'd
[30:51] Speaker 1: tell a lot of people to agree with that. Yeah,
[30:53] Speaker 1: that's the fear. Absolutely, it's a massive fear.
[30:56] Speaker 2: Yeah, and it's well founded. I think that the the
[31:00] Speaker 2: essence of being a human is our brain function, our
[31:03] Speaker 2: executive function, the fact that we're having this conversation now.
[31:07] Speaker 2: So when that is affected in any way, it has
[31:10] Speaker 2: massive implications and it's very hard for individuals and families
[31:15] Speaker 2: to cope with that.
[31:16] Speaker 1: So I just had to thought then if Matthew just
[31:19] Speaker 1: go back to something. When we're talking about high intensity exercise,
[31:24] Speaker 1: you can do that when you're forty, fifty, sixty, some
[31:28] Speaker 1: people maybe seventy, but it largely depends on your mobility
[31:32] Speaker 1: and a lot of other stuff, you know, energy levels,
[31:36] Speaker 1: et cetera. But when you're eighty does high intensity then? Mean?
[31:40] Speaker 1: I mean, how do we measure high intensity? Is it
[31:42] Speaker 1: about my heart as a percentage of maximum heart rate?
[31:47] Speaker 1: Or is it? And therefore you take one hundred and
[31:49] Speaker 1: two twenty multiply minus eighty and it gives me one
[31:52] Speaker 1: forty and I go, try you at eighty five percent
[31:55] Speaker 1: of that? Or is it? What is it? What is
[31:57] Speaker 1: high intensity? Well? That is exactly it.
[32:00] Speaker 2: But I suppose when you're eighty or ninety, are you
[32:02] Speaker 2: going to suddenly do a high intensity exer's for the
[32:04] Speaker 2: first time and do it as well as a twenty
[32:06] Speaker 2: year old. No, so you're going to be doing it
[32:08] Speaker 2: in your twenties, thirties, forties, fifties, sixty, seventies and eighties.
[32:11] Speaker 2: And in fact, by doing that, it makes it more
[32:13] Speaker 2: likely that you are going to be able to do
[32:14] Speaker 2: it in your eighties, nineties and one hundred. I see
[32:18] Speaker 2: a lot of people who come in who were in
[32:20] Speaker 2: fantastic health in their eighties and nineties. So that's the message.
[32:23] Speaker 2: You don't have to be in bad health, you don't
[32:25] Speaker 2: have to have you know, disability. But that hasn't come
[32:29] Speaker 2: out of nowhere. Yeah, So it's like doing homework all day,
[32:35] Speaker 2: every day for the course of your life.
[32:37] Speaker 1: Yes, and to that extent. And that's what this shows
[32:41] Speaker 1: a lot about this is that they you've got to
[32:43] Speaker 1: take control individuals. We might, but they're not going to
[32:46] Speaker 1: take control as someone makes them aware and sort of
[32:50] Speaker 1: give them a bit of an indication of the type
[32:52] Speaker 1: of life. There's life style of stuff. Yeah, change your life. No,
[32:55] Speaker 1: don't drink as much, don't drink it all if you
[32:58] Speaker 1: can help it, garettes at all, eat the right foods,
[33:02] Speaker 1: don't put on too much weight, exercise properly. Sleep is
[33:07] Speaker 1: really important. I do want to talk to you about
[33:11] Speaker 1: something this this APO like APO E. Chris Hemsworth did
[33:18] Speaker 1: he show on whatever whatever the streaming platform was. He
[33:23] Speaker 1: talked to Peter a teer Peter Tree blood test on
[33:26] Speaker 1: you know, one of the most athletic looking people and
[33:29] Speaker 1: I've ever seen on television. And I say, therefore, is
[33:32] Speaker 1: it athletic? He's young, And the bad news, as delivered
[33:37] Speaker 1: by Peter Tear to Hemsworth, was that he had two
[33:42] Speaker 1: alleles of E four one month from dad. I presume
[33:45] Speaker 1: he must have been my month for dad and he
[33:46] Speaker 1: was four E four. One could you comment on is
[33:53] Speaker 1: are we now testing for this stuff more more more often?
[33:58] Speaker 1: And two what does it mean?
[34:02] Speaker 2: Both excellent questions. We are testing for it more often,
[34:05] Speaker 2: but it's not routine and people often need to ask
[34:08] Speaker 2: for it. So I think it's important, and that's why
[34:10] Speaker 2: this show is important to understand that this is part
[34:13] Speaker 2: of a risk factor for conditions such as dementia. And
[34:19] Speaker 2: if you have alleles of APO E four, as you mentioned,
[34:22] Speaker 2: that means that you're less likely to break down the
[34:25] Speaker 2: proteins that cause dementia in the brain.
[34:28] Speaker 1: Because if that protein E four ye, or if it's
[34:33] Speaker 1: E two E three operates more efficiently than ethol. Absolutely,
[34:37] Speaker 1: that is that the issue. Yeah, And if you've got
[34:39] Speaker 1: A four, you don't have E two or three or
[34:42] Speaker 1: two in particular, you're not as likely to break down those,
[34:46] Speaker 1: so it's not that efficient in getting rid of all
[34:48] Speaker 1: the debris that's hanging around your brain.
[34:50] Speaker 2: Yeah, and it's still working, but it's not working as
[34:52] Speaker 2: well as I suppose the comparison of you know, nineteen seventies,
[34:56] Speaker 2: you know, Mini with a Tesla or something like that.
[34:59] Speaker 2: Like it's total different, but it is working to an extent.
[35:04] Speaker 2: So obviously, if you do have at BOI four like
[35:10] Speaker 2: Hemsworth's show on his show, that would put you at
[35:13] Speaker 2: a higher risk. So that would put more emphasis on
[35:16] Speaker 2: you to focus on all the other modifiable risk factors
[35:19] Speaker 2: that you can control, the ones that we've already talked about.
[35:23] Speaker 2: A statistical higher risk.
[35:24] Speaker 1: Yeah, it doesn't.
[35:27] Speaker 2: And these are based on and that's a good point.
[35:28] Speaker 2: These are based on populations. This is population health. However,
[35:32] Speaker 2: you can extrapulate the population to the best for you.
[35:37] Speaker 2: But of course an an equals one I e.
[35:39] Speaker 1: Yourself.
[35:40] Speaker 2: It's like it's not it's not an exact science.
[35:43] Speaker 1: Yeah. So, and as I understand it, there is something
[35:46] Speaker 1: like people who pass away with perhaps Alzheimer's disease or
[35:52] Speaker 1: some form of dementia, probably heart attacks two, but have
[35:57] Speaker 1: a ten times more of those people have the genotype
[36:03] Speaker 1: B four were both they've got both parents. It's a
[36:06] Speaker 1: ten time factor. So otherwise it's correlation it's not a causation.
[36:11] Speaker 1: But lets say, look, he looks great, I mean, and
[36:14] Speaker 1: obviously he's adjusted his lifestyle. And by the way, I
[36:16] Speaker 1: don't mind telling everyone, I'm me three E four. So
[36:18] Speaker 1: I got E four from one of my parents. I
[36:21] Speaker 1: don't know which one, but one of them, And I
[36:25] Speaker 1: don't know who to blame, so one mum or dad.
[36:27] Speaker 1: It doesn't really matter because they both passed away. But
[36:31] Speaker 1: point being is that there's a I don't know, six
[36:35] Speaker 1: times I don't have ten times chance like some other
[36:38] Speaker 1: statistical greater chance of having a brain disorder or even
[36:43] Speaker 1: a hard disorder, because the four actually fixed your heart too,
[36:45] Speaker 1: like it's a bad for your heart, and as you
[36:46] Speaker 1: always say, if it's not good for you with your brain,
[36:48] Speaker 1: E four does that too, and also has effect on
[36:50] Speaker 1: the kidneys. It's a kidney issue too, by the way,
[36:52] Speaker 1: because there's the same deal.
[36:54] Speaker 2: Absolutely the same deal, because as.
[36:56] Speaker 1: Your kidneys can get the archer can get, the ones
[37:01] Speaker 1: coming out of the kidney can get damaged because you're hardened,
[37:06] Speaker 1: and then they don't filter as well, and so you know,
[37:08] Speaker 1: you start getting early kidney disease. That's exactly. So it's
[37:12] Speaker 1: a big deal and we should be getting tests of
[37:14] Speaker 1: this sort of stuff more often. So E. Four just
[37:19] Speaker 1: explained a little bit more if you don't mind, because
[37:21] Speaker 1: one of the things that as I understand it, Matthew,
[37:24] Speaker 1: is that how comes after amyloid accumulation and TAO come
[37:32] Speaker 1: about as a result of other processes that happened before
[37:37] Speaker 1: that way before those things start getting produced. And there
[37:43] Speaker 1: is you know they're talking about, you know, the Crisper
[37:49] Speaker 1: process projects whereby they can turn some genes off that
[37:54] Speaker 1: some people have in their brain, whether they've got EPO
[37:57] Speaker 1: or not, that you can turn off these processes where
[38:01] Speaker 1: certain molecules are not going to get produced, which ultimately
[38:04] Speaker 1: end up in producing more amloids in tow Can you
[38:07] Speaker 1: just talk about your advances in crisper and what crisper is.
[38:11] Speaker 2: Well, first, I'd say that focusing on a particular gene
[38:16] Speaker 2: that might do one part of a function, that's great research,
[38:21] Speaker 2: but it might not necessarily have any impact or translation
[38:24] Speaker 2: into the humans that we are. So I think that's
[38:27] Speaker 2: the first thing. You often see these great discoveries, and
[38:29] Speaker 2: we've been able to model mice. Yeah, it did it on mice,
[38:32] Speaker 2: and you know, in a lot of the conditions we're
[38:34] Speaker 2: talking about. All of my studies have been negative because
[38:37] Speaker 2: how good is that model for the human disease?
[38:40] Speaker 1: Right?
[38:41] Speaker 2: And the other thing is we've obviously mentioned amyloid and
[38:45] Speaker 2: TAW and they're important parts, but they're not the whole
[38:47] Speaker 2: story either, and so there's a discussion. I remember when
[38:50] Speaker 2: people we talking about ammeloid they said, well, it's like
[38:52] Speaker 2: saying if you remove smoke, is at the end of
[38:55] Speaker 2: the fire.
[38:56] Speaker 1: No way.
[38:57] Speaker 2: So there's a whole process going on here. Emoloid and
[39:00] Speaker 2: TOW are critical parts, and the genes modifying them are
[39:04] Speaker 2: critical parts. But if we remove all of the amyloid
[39:07] Speaker 2: out of someone's brain, will they be back to normal? Well, no,
[39:10] Speaker 2: they're not, because we're doing that now. So we can
[39:13] Speaker 2: remove the amyloid with the monoclonal antibodies and they don't
[39:17] Speaker 2: get back to normal, they might either plateau or they
[39:19] Speaker 2: might might slow down the progression. But then the question
[39:23] Speaker 2: is can we find tune that when do we start it?
[39:26] Speaker 2: Do we start these medications at the age of thirty
[39:28] Speaker 2: when we see four is up and monitoring some other
[39:32] Speaker 2: parts of the biomus, and that's where we're going. We're
[39:34] Speaker 2: going to go earlier and earlier and earlier. And it
[39:37] Speaker 2: might be that one of the medications is related to
[39:40] Speaker 2: a gene modification in amyloid in a few years time,
[39:44] Speaker 2: but that's not available at the moment. The other thing
[39:47] Speaker 2: is when you start knocking out certain genes, you don't
[39:50] Speaker 2: know what the downstream effects of.
[39:51] Speaker 1: That effect is. Yeah, exactly. That might be good for
[39:55] Speaker 1: something else, yeah, and.
[39:56] Speaker 2: It might be a catastrophe, you know, were there were trials,
[39:59] Speaker 2: for instance, in Parkinson's disease, putting in stem cells into
[40:03] Speaker 2: the brain and all sounding great, It was looking good,
[40:05] Speaker 2: but then the stem cell started to overgrow and cause cancer,
[40:08] Speaker 2: and so people coming in with you know, overgrowth and
[40:12] Speaker 2: cancer cells in the brain. So it was a catastrophe.
[40:14] Speaker 2: So you've got to be able to understand. And that's
[40:16] Speaker 2: really why human trials are so critical. So a model
[40:21] Speaker 2: is only as good as a disease. It models, but
[40:24] Speaker 2: I think we have to get more and more into
[40:26] Speaker 2: patients and patients with neurological conditions. Of course we need
[40:31] Speaker 2: basic science and discovery, but we've got to focus on
[40:34] Speaker 2: the human.
[40:37] Speaker 1: We are talking. I mean, dementia covers a lot of
[40:40] Speaker 1: stuff and we've been talking about and Alzheimer is the
[40:42] Speaker 1: one probably everybody tends to focus on. But loss of memory,
[40:46] Speaker 1: I guess is probably of describing it. What is the
[40:50] Speaker 1: general progression? Though? From the moment you and I remember
[40:55] Speaker 1: asking you this question, I said to you, sometimes I
[41:00] Speaker 1: just can forget a word, and I just can't remember
[41:02] Speaker 1: the word, and about two or three minutes that comes
[41:06] Speaker 1: to me. Or I forget a person's name. I know
[41:07] Speaker 1: them so well, but I haven't said it maybe for
[41:10] Speaker 1: a while. And you said to me something like that
[41:13] Speaker 1: sort of anxiety memory because some of you are said
[41:17] Speaker 1: to me, oh my god, I can't remember that word.
[41:19] Speaker 1: And they're older people and they're going and they're just
[41:21] Speaker 1: marking around, go bloody, early dementia. But what what other
[41:26] Speaker 1: things could be causing us not to remember that the
[41:29] Speaker 1: name or the word. What is this anxiety about memory?
[41:34] Speaker 2: Well, I think once we start focusing on it, we
[41:35] Speaker 2: all become anxious. Like hearing a story there, I was
[41:37] Speaker 2: feeling a bit anxious, So that's something natural. But I
[41:41] Speaker 2: suppose you're worried that you can't recall a name or
[41:45] Speaker 2: a process, and then a little bit later you do,
[41:47] Speaker 2: so the function is there, so you haven't lost the function.
[41:51] Speaker 1: Right, ourzeime's major lost the function.
[41:53] Speaker 2: It doesn't doesn't come back right. And it's like I
[41:55] Speaker 2: suppose an onion starts stripping away the very core parts
[41:59] Speaker 2: of and remain and you might, you know, have memories
[42:02] Speaker 2: from long standing memories about you know, growing up and
[42:05] Speaker 2: your parents and so on, but you don't remember that
[42:07] Speaker 2: you need to go down and get you know, to
[42:09] Speaker 2: Col's and get dinner for tonight, those sort of things.
[42:12] Speaker 2: It's so there's a level of what is intrinsic in
[42:16] Speaker 2: your brain function that's laid down and these these are
[42:18] Speaker 2: memories that are laid down and reinforced. But it's the
[42:22] Speaker 2: short term issues that tend to be more problematic. And
[42:25] Speaker 2: that also means your daily function in your job, in
[42:29] Speaker 2: your family, in your environment.
[42:31] Speaker 1: So what is the usual progression? So people start having
[42:37] Speaker 1: maybe what's something that someone might come to you? And
[42:39] Speaker 1: obviously I don't want to breach any professional situation here,
[42:42] Speaker 1: but like maybe someone comes to you and like very
[42:47] Speaker 1: early stage Alzheimer's, like what would you what would you see?
[42:52] Speaker 2: Well, part of it can be prolonged word finding difficulties,
[42:55] Speaker 2: and we might test for it, like you might show
[42:58] Speaker 2: them a picture of say the Eiffel Tower and anyone.
[43:00] Speaker 2: So that's the Eiffel Tower, So what's that. That's that
[43:03] Speaker 2: place that's sort of not here, but it's and it's
[43:08] Speaker 2: it's made of metal, and they're sort of talking around,
[43:10] Speaker 2: so it's fluent, it's fluent speech, but they can't say
[43:14] Speaker 2: Eiffel Tower. They can't say that's a structure in powers
[43:16] Speaker 2: and Powers is in France. So the connections are all gone.
[43:19] Speaker 1: There are tests, specific tests later, Yeah, you'll.
[43:23] Speaker 2: Have them, and so either the neurologists will be involved
[43:26] Speaker 2: in those tests or there's a neuropsychologist. It's usually a
[43:29] Speaker 2: multidisciplinary approach and there's testing for word finding difficulties, but
[43:34] Speaker 2: also then trails, so for instance, doing networks of you know,
[43:38] Speaker 2: shapes and sizes, doing images of clocks, understanding times. Another
[43:44] Speaker 2: you know, test is verbal fluency. That's the frontal lobe function.
[43:48] Speaker 2: So for instance, I don't know if you want to
[43:50] Speaker 2: do it on the spot, but tell me all the letters,
[43:52] Speaker 2: all the words that you can think of with the letter.
[43:54] Speaker 1: M words real, masterclock, I can't even think he got
[44:04] Speaker 1: me nervous? Can I think of names? No? No, I
[44:09] Speaker 1: can't think of it. In addiction, money, metal, motor, car Modikaid, Mammoth, Milestone, mightiness, Michaelangelo.
[44:31] Speaker 1: How's my time going? Perfect?
[44:32] Speaker 2: You still got abut another ten or twenty seconds, But
[44:35] Speaker 2: more than more than double figures in a minute is normal?
[44:38] Speaker 1: Normal? Yeah? And also you're.
[44:40] Speaker 2: Looking at the words you use there, like like some
[44:42] Speaker 2: of those were three or four syllables, so they're very
[44:44] Speaker 2: complex words. So it's totally normal.
[44:46] Speaker 1: Yeah, but these are this is part of the So
[44:49] Speaker 1: how would someone know THATTT that they should go and
[44:51] Speaker 1: see someone? So because you know, like let's say I
[44:54] Speaker 1: could get to two out like for example, then I'm
[44:57] Speaker 1: sort of a bit late to the game. Talk to
[45:00] Speaker 1: a neurologist. Is there some sort of self testing? Is
[45:04] Speaker 1: there something like can they go to the new website
[45:07] Speaker 1: and your Your neuro website sort of explains a few
[45:10] Speaker 1: things to me and maybe it gets me starting to
[45:12] Speaker 1: think about it. Or I might be talking to my
[45:13] Speaker 1: brother who's younger than me, but I might have noticed
[45:16] Speaker 1: something I can say, maybe you just should go and
[45:18] Speaker 1: see a doctor about this. I mean, how far back
[45:20] Speaker 1: can we go?
[45:21] Speaker 2: Well, we have got risk assessment profiles through the neuro website,
[45:25] Speaker 2: and people can they're they're all free? Is that neuro
[45:27] Speaker 2: dot com dot you.
[45:28] Speaker 1: You, and.
[45:31] Speaker 2: I think it's also just your engagement in life, like
[45:33] Speaker 2: people like Sudoku's or reading the newspapers or you know,
[45:37] Speaker 2: looking at the stock market, talking about the the budget.
[45:41] Speaker 2: All of those sort of things are sort of that
[45:43] Speaker 2: that they're markers that things are going okay. The tests
[45:46] Speaker 2: that we're talking about are more buyer markers. Following a
[45:49] Speaker 2: clinical presentation, so someone has been brought in either on
[45:52] Speaker 2: their own volition or by by a family member or
[45:55] Speaker 2: a friend, like you know, Matthew's not not Matthew's not
[45:59] Speaker 2: the same person that he seemed to be, or there
[46:00] Speaker 2: seems to be some minor, like high level stuff, and
[46:03] Speaker 2: then we would go into this sort of cognitive assessment,
[46:06] Speaker 2: and then that cognitive assessment would suggest what we need
[46:09] Speaker 2: to do, Like it might say that actually part of
[46:11] Speaker 2: it as well is assessment of anxiety and mood. So
[46:15] Speaker 2: I might score badly, but it might be like really
[46:18] Speaker 2: really down in my in my mood score, and then
[46:22] Speaker 2: if I can improve my mood score, does the cognitive
[46:25] Speaker 2: process come out. And that's people use these word pseudo dementia,
[46:28] Speaker 2: so in other words, it's not really dementia, it's something
[46:31] Speaker 2: else that's triggering the process. We'd also then you know,
[46:35] Speaker 2: look at you know, blood test results, vitamin levels, thyroid function,
[46:39] Speaker 2: these are all markers that will help brain function and
[46:42] Speaker 2: they could account for the presentation wow.
[46:45] Speaker 1: And so like this whole an ecosystem around the outcome
[46:54] Speaker 1: is pretty important. It's not just one thing. It's not
[46:56] Speaker 1: just going to sit in front of your Olgers and
[46:57] Speaker 1: he goes, oh, you've got it or you got to
[47:00] Speaker 1: stage and what's the progress there? So, I mean, where
[47:03] Speaker 1: would someone end up. Let's say someone starts at seventy
[47:06] Speaker 1: either got early dementia and you know diagnosed, is it
[47:11] Speaker 1: ten years or fifteen years? A minute? And then how
[47:15] Speaker 1: are they at the end of it?
[47:16] Speaker 2: Well, the beauty is back to the autonomy issue. People
[47:19] Speaker 2: can have some control of the modifiable risk factor. So
[47:22] Speaker 2: let's say I was not scoring as well as I
[47:24] Speaker 2: should be, or I'd been measuring it over the last
[47:26] Speaker 2: ten years and I'm starting.
[47:27] Speaker 1: To drop off.
[47:28] Speaker 2: If I start to adjust some of my lifestyle factors
[47:32] Speaker 2: and some of the blood results I've got, can I
[47:35] Speaker 2: either plateau out or start to raise it again. And
[47:38] Speaker 2: these are things that yes, we can do. So when
[47:40] Speaker 2: you say is it ten years is at fifteen years. Well, no,
[47:43] Speaker 2: it's all modifiable. So forty five percent is modifiable. So
[47:47] Speaker 2: you've got control, right, So as long as you know that, yeah,
[47:51] Speaker 2: as long as you know so long as you've been
[47:52] Speaker 2: tested and as well, and part of that as well
[47:54] Speaker 2: blood pressure. So how often you get blood pressure checked
[47:56] Speaker 2: by a general practitioner if you're not seeing a general
[47:58] Speaker 2: practition again see practition to get your blood pressure.
[48:01] Speaker 1: Gown by one of those omor on things what they're
[48:03] Speaker 1: called from the chemist. So I go one a home
[48:05] Speaker 1: just every day. Probably it would be great if because
[48:08] Speaker 1: somehow I talked to my phone there could be some
[48:10] Speaker 1: sort of app to it that I could actually you
[48:13] Speaker 1: probably can get it minds old, but actually I can
[48:15] Speaker 1: have a record of I can actually see the changes.
[48:17] Speaker 1: But that's happening. It's a hundred bucks because a hundred
[48:20] Speaker 1: bucks and the whole family can use it and you
[48:23] Speaker 1: can use it forever and so but in the end,
[48:28] Speaker 1: what is a person from dementia die from? Very good question.
[48:33] Speaker 2: It doesn't kill them, does it? Well, it does, but
[48:36] Speaker 2: it's back to the brain is the sort of executive
[48:40] Speaker 2: function controlling all other organs. So usually part of that
[48:44] Speaker 2: is you're breathing, so you don't necessarily, you know, breathe
[48:47] Speaker 2: as as quickly and as deeply as normal, so that
[48:51] Speaker 2: you know the base of the lungs don't fill up
[48:53] Speaker 2: with air as they normally do. Some fluid might stay
[48:56] Speaker 2: down there. You might aspirate, so you might swallow your
[48:59] Speaker 2: food incorrectly. There'll be a chest infection. You die for pneumonia,
[49:02] Speaker 2: So you die for pneumonia. That's the most common. But alternatively,
[49:05] Speaker 2: it also does control you know, your heart, your heart rhythm.
[49:08] Speaker 2: People have heart attacks that they just die in their sleep.
[49:11] Speaker 2: So the brain is controlling all of these functions. But yeah,
[49:14] Speaker 2: that's how you die.
[49:16] Speaker 1: As you know, my mother was went to the other
[49:20] Speaker 1: place you used to be at Brandon Mind Center when
[49:22] Speaker 1: she had motor neurone disease, and she died of motor
[49:25] Speaker 1: neurone disease. And it's a it's a crappy way to die,
[49:29] Speaker 1: to be honest, it's one of the worst. I've seen
[49:31] Speaker 1: lots of people pass away and that's the worst thing
[49:33] Speaker 1: I've ever seen. Motor neurone disease is different to dementia.
[49:41] Speaker 1: And say, someone like me, who's you know, I've had
[49:45] Speaker 1: lots of concussions, mini concussions, and major concussions. Is there
[49:51] Speaker 1: any scientific evidence or statistical evidence about and that correlates
[49:59] Speaker 1: concussions to als or motori disease.
[50:03] Speaker 2: Yeah, Well, just to put it into a bit of perspective, So,
[50:07] Speaker 2: motor neurone disease is a neurodegenerative condition. A neurodegeneration incorporates dimension.
[50:12] Speaker 2: Dementia is due to say Alzheimer's disease or vascular dimension
[50:16] Speaker 2: that we've talked about. Modeor neurine disease is due to
[50:19] Speaker 2: a protein abnormality in the brain as well, called TDP
[50:22] Speaker 2: forty three. It tends to affect particularly the motor pathway,
[50:26] Speaker 2: so the cordico spinal tract, which is a tract that
[50:29] Speaker 2: goes through the brain and spinal col cord and controls
[50:33] Speaker 2: all of our voluntary muscles. So the motor neurine itself
[50:36] Speaker 2: is one of the biggest cells in the body. Sometimes
[50:39] Speaker 2: it's up to one point four meters long and has
[50:41] Speaker 2: huge metabodys one point one point four meters. It's huge,
[50:46] Speaker 2: that's massive, massive, but it has high metabolic needs and
[50:50] Speaker 2: it means what it requires a lot of, you know, protein.
[50:55] Speaker 2: It's very sensitive to not having things, you know, waste
[50:57] Speaker 2: cleared out properly, so it needs you know, all the
[51:00] Speaker 2: things we've talked about healthy sleeping habits are good protein,
[51:04] Speaker 2: good nutrition, and exercise. But for what for some individuals
[51:09] Speaker 2: in the community, they're prone to having a disease whereby
[51:14] Speaker 2: the degeneration occurs in the mode and urine itself, and
[51:18] Speaker 2: so people start to develop weakness. It's usually focal. So
[51:22] Speaker 2: in our clinics, I think we give a picture of
[51:25] Speaker 2: a human and we so where did the disease begin?
[51:27] Speaker 2: And they can always pinpoint whether it began in my
[51:29] Speaker 2: right hand, whether it began in my mouth, where it
[51:32] Speaker 2: began in my.
[51:32] Speaker 1: Left legatis the patient.
[51:34] Speaker 2: So it always begins, it seems to begin in one
[51:37] Speaker 2: area and then it starts to spread and become a
[51:40] Speaker 2: bit more generalized.
[51:41] Speaker 1: So just explain where that cell is that one point
[51:44] Speaker 1: four meter.
[51:46] Speaker 2: So it starts in the brain and goes all the
[51:49] Speaker 2: way down through the spinal cord, and then there's what
[51:51] Speaker 2: we call a sign apse to what we call the
[51:54] Speaker 2: lower mode in urine, which comes out and goes into
[51:57] Speaker 2: the nerve for instance, of your arm or your leg,
[51:59] Speaker 2: or into the tongue.
[52:00] Speaker 1: So long skinny cellars that must be quite skinny if
[52:03] Speaker 1: it's going down. Yeah, we'll talk about microscopic. Yeah, microscope,
[52:06] Speaker 1: but it's always get one point four meters in length
[52:10] Speaker 1: up to one point four death. Wow.
[52:12] Speaker 2: But it controls everything you're doing now, like talking, moving
[52:15] Speaker 2: your hands.
[52:15] Speaker 1: Your leg. So it's not your brain that does it,
[52:17] Speaker 1: it's the well.
[52:18] Speaker 2: The control is through the brain and central the central
[52:21] Speaker 2: mode of neurine is there in the brain.
[52:23] Speaker 1: Right, and and that's the thing that controls all your
[52:26] Speaker 1: motor motor skills what are you want to call it?
[52:28] Speaker 1: And and so just going back a step on that,
[52:34] Speaker 1: I remember one of the things they did to my
[52:37] Speaker 1: mother's they were they did it on the hands. They're
[52:39] Speaker 1: putting pins in it like I don't know, stimulating her
[52:42] Speaker 1: hand Yep, that's how she got diagnosed.
[52:45] Speaker 2: Yeah, So neurophysiology is the critical part of a diagnosis.
[52:49] Speaker 2: That's that's the investigation. And nerves and muscles are electrically active,
[52:55] Speaker 2: so the signals going down through the nerve that go
[52:58] Speaker 2: to the muscle that keeps the muscle live. If the muscle,
[53:01] Speaker 2: if the nerve is damaged, the muscle starts firing off
[53:04] Speaker 2: by itself, and a manifestation of that might be muscle twitching.
[53:08] Speaker 2: But if we put a needle into the muscle and
[53:11] Speaker 2: it's firing off by itself, so in other words, the
[53:14] Speaker 2: patient isn't controlling it's going. It's just firing units going
[53:17] Speaker 2: bang bang bang bang bang. That's a feature of nerve
[53:21] Speaker 2: damage to that particular muscle.
[53:23] Speaker 1: Now, if, for.
[53:23] Speaker 2: Instance, you know you're working as a butcher and you
[53:26] Speaker 2: accidentally cut the nerve and that muscle was affected, that
[53:29] Speaker 2: makes sense. But if I start putting needles into lots
[53:32] Speaker 2: of different areas and getting the same results, it suggesting
[53:35] Speaker 2: there's a more widespread abnormality of nerve and muscle function,
[53:39] Speaker 2: and that's what is typically the picture of modeer neurine disease.
[53:43] Speaker 2: So with your mother, it'll be testing muscles in the
[53:46] Speaker 2: arms and the legs and the speech muscles, and if
[53:48] Speaker 2: they're all affected, that's, you know, that's the sign of
[53:52] Speaker 2: modern neurine disease.
[53:53] Speaker 1: So her first sign of there being a problem was
[53:58] Speaker 1: that I used to ring her every night, so I'll
[54:02] Speaker 1: be going home and my way home from work on
[54:04] Speaker 1: ring her. My mother loves to speak talk a lot,
[54:06] Speaker 1: and she's a Orish descent, so Irish people love to
[54:10] Speaker 1: have a chat, so I would recall the moment I
[54:12] Speaker 1: got my car, because I knew it was twenty five
[54:14] Speaker 1: minutes to get home, so I could sort of limit
[54:16] Speaker 1: the time and say, mom my home, Now I'm going
[54:17] Speaker 1: to have a dinner. So but I noticed she didn't drink.
[54:21] Speaker 1: I noticed that she started to sound like she was drunk,
[54:25] Speaker 1: not drunk, but slurring her words, like a person who
[54:28] Speaker 1: has been drinking would sound not bad, but just a
[54:30] Speaker 1: little bit slurring. And she was always very articular. And
[54:34] Speaker 1: I said to her, are you drinking, like having a
[54:36] Speaker 1: whisky with dad or something like that, and she said no, no, no,
[54:40] Speaker 1: And then that's when we decided to get her checked out.
[54:45] Speaker 1: Does it normally start off in the speech, So.
[54:49] Speaker 2: There's three areas really were a beginning, So it's usually
[54:52] Speaker 2: upper limonset is the most common, so in your arms,
[54:55] Speaker 2: then lower leg so leg weakness is the second, and
[55:00] Speaker 2: speech is the third, so you call it bulbar onset.
[55:03] Speaker 2: So it's the tongue muscle, so the tongue has become weak.
[55:05] Speaker 1: So she would have had those other things before.
[55:08] Speaker 2: Necessarily, so it can begin in the mouth. And I
[55:11] Speaker 2: suppose it's interesting that humans are the only ones who
[55:15] Speaker 2: have a form of communication like speech, and that's also
[55:18] Speaker 2: an are that that's where mode neurone disease begins. Another
[55:22] Speaker 2: area where it begins is the pincer grip in the hand,
[55:24] Speaker 2: and we're the only mammalian species who can do a
[55:27] Speaker 2: pincer grip. But then when you look at the motors
[55:29] Speaker 2: strip in the brain, the two biggest areas they have
[55:32] Speaker 2: massive representation are the bulbar region and the thumb and
[55:36] Speaker 2: the index finger the bulbarth Yeah, so that's been evolution.
[55:41] Speaker 2: Our brains have grown in those regions so that we
[55:43] Speaker 2: can speak, we can do this pincer grip. But as
[55:47] Speaker 2: a result, it's got huge metabolic demand. And when there's
[55:50] Speaker 2: a failure of that network, how does it manifest? Speech
[55:53] Speaker 2: goes off or upper limb function, particularly pincer grip is diminished.
[55:58] Speaker 1: So has the disease has got something to do with
[56:01] Speaker 1: the metabolic demand not being satisfied? Yeah, or is it?
[56:08] Speaker 1: Let's rule genetics out. Is it because the metabolic demand
[56:13] Speaker 1: is not being met In other words, I'm neither not
[56:16] Speaker 1: a blood flying there, but no of nutrients getting in there?
[56:19] Speaker 1: What is it?
[56:20] Speaker 2: Most likely that is the case, and there's a probably
[56:23] Speaker 2: a threshold what gets something over a threshold for an abnormality,
[56:27] Speaker 2: and it's probably cellular failure and that leads to a
[56:31] Speaker 2: protein abnormality, a folding protein abnormality in this case TDP
[56:35] Speaker 2: forty three. And that's then that we use the word
[56:39] Speaker 2: notice it's the origin, and then the origin starts to
[56:42] Speaker 2: spread out like a fire spreading through the brain or
[56:45] Speaker 2: through the motor pathways.
[56:48] Speaker 1: And are there any treatments yet.
[56:52] Speaker 2: Well, in terms of why individuals get it, we know
[56:56] Speaker 2: that there's genetic abnormalities and there's been large study has
[57:00] Speaker 2: been one study that was done here in Australia and
[57:03] Speaker 2: in Japan and Korea showing that they needed to be
[57:07] Speaker 2: six things to happen for someone to develop mode of
[57:10] Speaker 2: neurone disease, six hits and if there is a gene
[57:14] Speaker 2: in the family that accounts for three of the hits,
[57:17] Speaker 2: then the other three are at this stage unknown.
[57:21] Speaker 1: But if there is.
[57:22] Speaker 2: A genetic abnormality, there is now genetic treatment so to
[57:25] Speaker 2: first one was approved in May of this year twenty
[57:28] Speaker 2: twenty six, that's now available to treat superoxide dismutes one
[57:32] Speaker 2: SOD one genetic forms of als. Then we have neuroprotective therapy.
[57:37] Speaker 2: So really zola is available and that was through clinical
[57:40] Speaker 2: trials that we were actually part of in the mid
[57:42] Speaker 2: nineteen nineties and that was approved in Australia in twenty
[57:45] Speaker 2: twenty five, two thousand and five. And the second medication
[57:49] Speaker 2: is a darovone already kava, which is an intravenous infusion,
[57:53] Speaker 2: and that was approved in twenty twenty five. So the
[57:55] Speaker 2: other three approved the medications in a space you've got it.
[57:58] Speaker 1: Yeah, So it's and what's and what's its success rate
[58:01] Speaker 1: like efficacy in terms.
[58:03] Speaker 2: Of well, the idea is to keep people in the
[58:05] Speaker 2: mildiforms for longer and so the patients are living with
[58:08] Speaker 2: the disease for a longer period of time, less affected.
[58:12] Speaker 1: Right. So, but you mentioned with some forms of dementia
[58:17] Speaker 1: that there are lifestyle actors that can improve dementia. Other
[58:20] Speaker 1: lifestyle actors can improve.
[58:23] Speaker 2: Well some of the factors that are still relevant. But
[58:25] Speaker 2: you know, in physical exercise but not too much. And
[58:29] Speaker 2: there has been, I suppose an understanding that sports people
[58:34] Speaker 2: are more commonly affected. So for instance, in America, it's
[58:37] Speaker 2: called Lugerrig's disease. Lugeeric developed als in his thirties and
[58:42] Speaker 2: obviously we've seen a lot of tennis players, Brad Drewett,
[58:47] Speaker 2: Peter Dowen, We've seen rugby players have been affected. So
[58:53] Speaker 2: this AFL Neil Danaher, who's totally Neil Danaher and Fighter
[58:58] Speaker 2: and D are the third largest unders of modern neurone
[59:01] Speaker 2: disease research globally, Like, isn't that amazing from Australia And
[59:06] Speaker 2: who's the other fight M and D which is what
[59:08] Speaker 2: he established.
[59:09] Speaker 1: Wow, third biggest in the world. In the world. Yeah,
[59:13] Speaker 1: it's amazing. That's fantastic. It's fantastic.
[59:16] Speaker 2: So what are the some of the lifestyle things though,
[59:19] Speaker 2: Matthew like, well, these are complicated discussions, but certainly we
[59:24] Speaker 2: know that head injuries form part of that discussion. And
[59:29] Speaker 2: there was a study that came out a couple of
[59:31] Speaker 2: years ago showing higher incidences of neurodegenerative diseases, including mode
[59:35] Speaker 2: neurone disease in contact athletes, particularly professional high level contact.
[59:40] Speaker 1: Athletes like NFL and stuff like that.
[59:42] Speaker 2: Yeah, yeah, yeah, And I think that the study came
[59:44] Speaker 2: I think from the Scottish brain banks, so they've had
[59:47] Speaker 2: a lot of Scottish rugby union players and they made
[59:51] Speaker 2: that connection. It's similar here. And I know that the
[59:54] Speaker 2: Rugby codes are very interested and they're very concerned about it,
[59:57] Speaker 2: and they're putting a lot of focus on it in
[1:00:00] Speaker 2: the AFL and the NRL to try and understand these
[1:00:02] Speaker 2: conditions better. But it's a form of research, so we
[1:00:07] Speaker 2: still don't have, you know, one hundred percent diagnostic approach
[1:00:10] Speaker 2: for chronic traumatic and caphilopathy CTE, and part of that
[1:00:15] Speaker 2: is really diagnosed by doing the post mortem examination.
[1:00:19] Speaker 1: Maybe you could explain it because a lot of people
[1:00:20] Speaker 1: come and say I've been I've heard them, I know them,
[1:00:24] Speaker 1: I've been diagnosed with the CTE, And as I understand it,
[1:00:27] Speaker 1: you can't do that until you actually get hold of
[1:00:29] Speaker 1: their brain once they passed away to do the actual diagnosis.
[1:00:32] Speaker 2: That's exactly it, and every approach that's been used up
[1:00:35] Speaker 2: till now has been unsuccessful. And in whole groups where
[1:00:39] Speaker 2: people said, oh there's a ct and they go and
[1:00:41] Speaker 2: to the postmodern examination, there's no neuropathological evidence of ct.
[1:00:45] Speaker 1: Maybe you could explain what it looks like. I've seen
[1:00:47] Speaker 1: it because I've been to the brain bang at it
[1:00:50] Speaker 1: a Brain of Mind center, and in fact I made
[1:00:53] Speaker 1: a big donation and then said to them they can
[1:00:55] Speaker 1: have my brain when I pass away if they want
[1:00:58] Speaker 1: to do evenuevary. But they showed me when it was
[1:01:01] Speaker 1: actually like a so here's your brain, like you know,
[1:01:05] Speaker 1: that's sort of wrinkly sorting and there was a big
[1:01:08] Speaker 1: sort of dent like that is that is that? Am I? Right? So?
[1:01:11] Speaker 2: Look there are holes in the brain where fluid passes
[1:01:15] Speaker 2: through and they become bigger, and the cell the cell
[1:01:18] Speaker 2: processes of the brain becomes smaller, so they shrink, so
[1:01:21] Speaker 2: you get shrinkage of different areas. You can also get
[1:01:23] Speaker 2: then it's like scar tissue building up in the brain
[1:01:27] Speaker 2: and the space has become bigger. That's and then there's
[1:01:29] Speaker 2: certain patterns.
[1:01:31] Speaker 1: But but why can't you look at that under an
[1:01:33] Speaker 1: MRI or a machine.
[1:01:35] Speaker 2: Well, there are so many other things that could also
[1:01:36] Speaker 2: be affecting the brain, right, I think though that it's
[1:01:40] Speaker 2: really interesting that I think we're going to get better
[1:01:43] Speaker 2: by using the technology of the day. So AI with
[1:01:46] Speaker 2: hundreds of thousands of scans is much better than you
[1:01:50] Speaker 2: or I looking at a scan and saying it looks
[1:01:52] Speaker 2: normal or it doesn't look normal like that. That's that's
[1:01:55] Speaker 2: where're at today. That's all going to be a thing
[1:01:57] Speaker 2: of the past.
[1:01:58] Speaker 1: Like the guys from Harris and AI, those guys who
[1:02:01] Speaker 1: are producing all these AI models to assist the radiologist, yes,
[1:02:06] Speaker 1: and the neurologists in your case, in his or her diagnosis.
[1:02:11] Speaker 2: And that's a global approach. And at neuro we're hopeful
[1:02:14] Speaker 2: of signing up a partnership with IMAD and using the
[1:02:18] Speaker 2: sort of the volume of practices they have to use
[1:02:20] Speaker 2: AI technology to better diagnose all of the conditions we've
[1:02:24] Speaker 2: been talking about, you know, today, and that's going to
[1:02:26] Speaker 2: be the reality. But then also can we go earlier
[1:02:31] Speaker 2: and at the moment we can't. But let's say we
[1:02:34] Speaker 2: did a brain health check of a thirty year old.
[1:02:36] Speaker 2: We wouldn't do an MRI scan because what are we
[1:02:39] Speaker 2: going to find And what we don't want to do
[1:02:41] Speaker 2: is find an incidental finding. Let's say there's a little
[1:02:43] Speaker 2: cyst in the brain, what should we do about that?
[1:02:46] Speaker 2: And the current understanding of incidental findings is leave them alone?
[1:02:50] Speaker 2: Like that just leads to a whole you know, you
[1:02:52] Speaker 2: mentioned anxiety, and you imagine the anxiety of the patient,
[1:02:55] Speaker 2: of the treating doctor of the family. Do you intervene
[1:02:58] Speaker 2: or nind is to not intervene, leave it alone. You
[1:03:02] Speaker 2: didn't do the scan to find that that's an incidental finding.
[1:03:05] Speaker 1: But maybe you do go back in five years time
[1:03:07] Speaker 1: to see if there's been in delta any change. Exactly
[1:03:10] Speaker 1: that's your delta. That's good, I don't you said, well,
[1:03:13] Speaker 1: but yes, that's exactly it. Yeah, yeah, because as you
[1:03:15] Speaker 1: know how to preneuvo. And the only reason I had
[1:03:18] Speaker 1: it was not to get well. I did take it
[1:03:21] Speaker 1: to you, and I took it to live specially took
[1:03:22] Speaker 1: with everybody, but everybody was fine. But the point being
[1:03:26] Speaker 1: here is now Prinivas or Australia, I mean I can
[1:03:28] Speaker 1: go and get another one, and I presume they've got
[1:03:31] Speaker 1: own their own AI systems. Now they could probably look
[1:03:33] Speaker 1: at both of them, but I can someone can They
[1:03:36] Speaker 1: can say well that has grown. So like one of
[1:03:40] Speaker 1: the things you pointed out to me in relation to
[1:03:42] Speaker 1: the scan of my brain when I had my whole
[1:03:44] Speaker 1: body was I think you said, I think you use
[1:03:47] Speaker 1: the word plak be used as normal because for my age,
[1:03:52] Speaker 1: but if that was like double in a year or two,
[1:03:55] Speaker 1: then you said, well, hang on, let's have a little.
[1:03:57] Speaker 2: Bit of that. It's the yeah, and that could be
[1:03:59] Speaker 2: getting part the threshold to intervene.
[1:04:02] Speaker 1: Yeah, yeah, so I'm actually going to go and get
[1:04:04] Speaker 1: another one. But I think down in Melbourne, it's what
[1:04:07] Speaker 1: do you think about I mean, I know it's expensive,
[1:04:10] Speaker 1: and you know it's easy for me to say, but
[1:04:14] Speaker 1: what do you think about those sorts of processes as
[1:04:17] Speaker 1: a brain doctor us getting and you can get it
[1:04:22] Speaker 1: an your brain much cheaper than a whole reneuvo? But
[1:04:26] Speaker 1: what about what do you think about people doing that?
[1:04:27] Speaker 1: As a market say at six years of age? Should
[1:04:31] Speaker 1: they think about that sort of stuff?
[1:04:33] Speaker 2: Well, look, I'm a scientist and I love the brain. Yeah,
[1:04:36] Speaker 2: I love all of this sort of stuff.
[1:04:38] Speaker 1: You a scientists first or a clinician?
[1:04:41] Speaker 2: What do you I'd say clinician your clinician, as in
[1:04:44] Speaker 2: you diagnose and examine and prescribe. But we all want
[1:04:47] Speaker 2: we all want better outcomes and where's that going to come.
[1:04:50] Speaker 2: That's going to come from the science.
[1:04:51] Speaker 1: And I think you need to explain that though. I
[1:04:53] Speaker 1: think most people don't know the difference between a brain scientist,
[1:04:56] Speaker 1: a neuroscientist, and a neurologist. I mean, what are the
[1:05:00] Speaker 1: different roles and they know different things? True?
[1:05:04] Speaker 2: Well, look I suppose in you're a neurologist is a
[1:05:09] Speaker 2: doctor so you do you do medical training. A scientist
[1:05:12] Speaker 2: does a science degree and they might focus on neurosciences
[1:05:16] Speaker 2: and they might focus on a part of neuroscience, could
[1:05:19] Speaker 2: be synapses, it could be on the pure mathematics, it
[1:05:22] Speaker 2: could be unstructural.
[1:05:23] Speaker 1: But I think.
[1:05:25] Speaker 2: It's science unlocks the understanding. And at the beginning we
[1:05:29] Speaker 2: talked about brain, you know, being their number one. We're
[1:05:32] Speaker 2: careful about saying, you know, you know, cause of death
[1:05:35] Speaker 2: in Australia. But to try and turn that around, we
[1:05:38] Speaker 2: need people focusing on the science and why has that happened,
[1:05:41] Speaker 2: and that could be anything from epidemiology, population studies, what's
[1:05:45] Speaker 2: happening in you know, Sydney compared to Perth versus rural Australia.
[1:05:50] Speaker 2: That's all science, and then by trying to take that
[1:05:53] Speaker 2: forward to try and have a message to try and
[1:05:56] Speaker 2: improve outcomes, ideally outcomes for a pop but then also
[1:06:01] Speaker 2: outcomes for an individual.
[1:06:03] Speaker 1: And they're any exciting maybe a tablet or whatever it
[1:06:08] Speaker 1: is exciting things on the you know out there in
[1:06:12] Speaker 1: the future that you know of that you guys might
[1:06:16] Speaker 1: be looking at, like testing or whatever the case may be,
[1:06:19] Speaker 1: for things like dementia. And we'll just leave manual disease
[1:06:23] Speaker 1: leave aside, but what about dementia.
[1:06:25] Speaker 2: Well, look, I think one of the most exciting things
[1:06:27] Speaker 2: that's happened in medicine over the last few years has
[1:06:31] Speaker 2: been the GLP one so glucagan like peptides, and these
[1:06:36] Speaker 2: have come out of particularly the realm of sugar controlled
[1:06:39] Speaker 2: blood sugar diabetes, and they're just so incredibly effective.
[1:06:45] Speaker 1: Being ozembic for example, yeah, or mandura or whatever it's called,
[1:06:49] Speaker 1: those those things.
[1:06:50] Speaker 2: So it actually came from very interesting research showing that
[1:06:52] Speaker 2: if you put if you had glucose, either you ingested
[1:06:55] Speaker 2: it or injected it, they had different levels in the body.
[1:06:59] Speaker 2: So it turns out if you ingested that something was
[1:07:02] Speaker 2: released that actually brings the blood sugar levels down much
[1:07:05] Speaker 2: better than if you had sugar injected. And it took
[1:07:09] Speaker 2: a while that that was called gligan like peptide, so
[1:07:13] Speaker 2: GLP GLP one, But GOLP one only survives in the
[1:07:17] Speaker 2: body for a few minutes after you eat a meal. Really, yeah,
[1:07:21] Speaker 2: so it's not really the stuff you produce. Yeah, it
[1:07:25] Speaker 2: turns out there was this endocrinologist and he's working for
[1:07:28] Speaker 2: the Veterans Affairs and they said, look, go and you know,
[1:07:30] Speaker 2: try and work on this area in general, as they
[1:07:33] Speaker 2: just went through virtually like encyclopedias. And he found this
[1:07:36] Speaker 2: thing called a Gila monster, and a Gila monster had
[1:07:39] Speaker 2: pancreatic overgrowth but also could slow their metabolism down and
[1:07:45] Speaker 2: manage blood sugar control. And so he off line. He
[1:07:49] Speaker 2: went and found some of the venom of this Gila monster,
[1:07:51] Speaker 2: and then he animals it.
[1:07:52] Speaker 1: Was a national animal, yeah, g LA.
[1:07:55] Speaker 2: And he found a new substance called extendon, and extendon
[1:08:00] Speaker 2: looked like glucagan like peptide, and he thought this could
[1:08:05] Speaker 2: be the key. So he went back to his bosses
[1:08:07] Speaker 2: at Veterans' Affairs and he said, look, I think I
[1:08:09] Speaker 2: found something. And I said, look, it's not relevant for us,
[1:08:11] Speaker 2: because we're only interested in veterans, more interested in you know,
[1:08:14] Speaker 2: blast Day's spinal cord injury. We're not interested in this
[1:08:17] Speaker 2: sort of stuff. But he thought he's onto something, so
[1:08:19] Speaker 2: he patented himself. He had to put a take a
[1:08:23] Speaker 2: loan out on the house, and then basically it was
[1:08:27] Speaker 2: becoming very, very expensive. So he then went and presented
[1:08:29] Speaker 2: at the American Diabetes Association, and a person from a
[1:08:34] Speaker 2: small therapeutics company, Ammelon came along and thought this is fascinating,
[1:08:38] Speaker 2: called up his bosses that straight away and they came
[1:08:42] Speaker 2: up to a licensing agreement that was eventually then taken
[1:08:45] Speaker 2: on with Lily. And that is the whole GLP one.
[1:08:49] Speaker 2: So extendon would turn GLP one instead of disappearing within
[1:08:54] Speaker 2: a few minutes, could make it last in the body
[1:08:56] Speaker 2: for hours four to twenty four hours. And this all
[1:08:58] Speaker 2: came from the skill was that a lizard. So I
[1:09:01] Speaker 2: suppose that also shows discoveries come from anywhere. But you've
[1:09:04] Speaker 2: got to have curiosity, the curiosity like this guy thought, oh,
[1:09:08] Speaker 2: this is interesting. There's a lizard that has a big
[1:09:11] Speaker 2: pancreas that must be doing something about, you know, blood
[1:09:13] Speaker 2: sugar control. And that's where it's all come from.
[1:09:16] Speaker 1: And where is GOLP one fit into Brainhill? Now got
[1:09:20] Speaker 1: distracted there for a lot now, but it was a
[1:09:22] Speaker 1: great story. I love it.
[1:09:23] Speaker 2: But what's very interesting is that GP one was used
[1:09:26] Speaker 2: for blood sugar control and in the studies that and
[1:09:29] Speaker 2: this is all you know. Publishing the best journals of
[1:09:31] Speaker 2: the world, New England Journal of Medicine, landst et cetera.
[1:09:34] Speaker 2: They're also now seeing that cognitive function is improved in
[1:09:38] Speaker 2: diabetics treated with this family of medications.
[1:09:42] Speaker 1: So that's established.
[1:09:43] Speaker 2: So if you have altered blood sugar control and you
[1:09:46] Speaker 2: get treated with these medications, you preserve brain health as
[1:09:50] Speaker 2: opposed to not having the treatment. Now the next question is, Okay,
[1:09:54] Speaker 2: they're in diabetic patients. What about patients with anonymer disease. Yeah,
[1:09:58] Speaker 2: and so that's cutting ENGINEW. So the t I was
[1:10:00] Speaker 2: underway in Alzum's disease with GLP one, and I think
[1:10:04] Speaker 2: this is where it's really going to start breaking open.
[1:10:07] Speaker 2: And again we're going to see the importance of metabolic health,
[1:10:09] Speaker 2: brain health, frailty all coming together. But then the individual
[1:10:13] Speaker 2: GP is going to be able to unlock all of
[1:10:15] Speaker 2: this with the markets coming from the patient. So it's
[1:10:18] Speaker 2: going to be fascinating, but I think it's going to
[1:10:21] Speaker 2: really improve our outcomes as a community.
[1:10:24] Speaker 1: So and GLP one like originally was marketed or is
[1:10:30] Speaker 1: that because originally marketed for a bit like a lot
[1:10:32] Speaker 1: of people us lose weight and not originally but like
[1:10:34] Speaker 1: after that, but when it got into the consumer world,
[1:10:37] Speaker 1: the retail world, and how does it stop you from
[1:10:41] Speaker 1: putting weight on? What's it make? I thought it'd stop
[1:10:44] Speaker 1: your appetitis something.
[1:10:45] Speaker 2: It does work on appetite, but it also works on
[1:10:48] Speaker 2: emptying of the of your stomach of food. But the
[1:10:52] Speaker 2: effects through brain health are also linked to the effects
[1:10:55] Speaker 2: on obesity, reducing inflammation, reducing sleep, and when you have
[1:11:01] Speaker 2: less sleep, aap near the glymphatic system is working. It's
[1:11:04] Speaker 2: clearing up the proteins at night time. So it's all
[1:11:07] Speaker 2: We're all a huge ecosystem.
[1:11:10] Speaker 1: And that's my final question or my final sort of
[1:11:13] Speaker 1: subtopic I wanted to talk about. With sleep. Everyone sleeps,
[1:11:21] Speaker 1: we all need different levels of sleep, and of course
[1:11:24] Speaker 1: everyone keeps saying you got to sleep from seven eight hours,
[1:11:26] Speaker 1: but I mean it's rare that I ever ever do that.
[1:11:29] Speaker 1: I might be bed for that long, but I might
[1:11:31] Speaker 1: not sleep that whole period. What is the difference between, Well,
[1:11:35] Speaker 1: why is it important from a brain health point of
[1:11:37] Speaker 1: view to a get overall enough sleep but be consistently
[1:11:44] Speaker 1: to do it and c also to have slow wave
[1:11:49] Speaker 1: sleep or what they call deep sleep or restored sleep
[1:11:52] Speaker 1: not so much round but the other one. What is
[1:11:55] Speaker 1: that doing for our brain?
[1:11:58] Speaker 2: So this is again an evolving era of side. But
[1:12:00] Speaker 2: understanding that there are systems in the brain that switch
[1:12:03] Speaker 2: on when we're in sleep and deep sleep, and we
[1:12:06] Speaker 2: need that every day to clean out the abnormalities, the
[1:12:10] Speaker 2: protein abnormalities. In particular, we've talked about amyloid TAO, but
[1:12:13] Speaker 2: presumably TDP forty three ouphas on newclin they've been pushed
[1:12:17] Speaker 2: through this sort of cleansing process during us sleep. Now,
[1:12:21] Speaker 2: the question I suppose when someone does have a sleep
[1:12:23] Speaker 2: abnormality is is it a sleep abnormatic abnormality that's been
[1:12:27] Speaker 2: driven by brain function or is it just a lifestyle problem.
[1:12:30] Speaker 2: And it's much better to try and address that early on.
[1:12:33] Speaker 2: And we all need proper sleep and whatever that hour
[1:12:36] Speaker 2: those hours are is everyone's different. Like you said, you know,
[1:12:40] Speaker 2: you don't need eight hours, and that's true. Some people
[1:12:42] Speaker 2: need five, six, seven. But we all need a certain quality,
[1:12:46] Speaker 2: a certain amount of sleep, but also than a deep sleep,
[1:12:49] Speaker 2: and this is for preserving brain function.
[1:12:52] Speaker 1: And deep sleep. During that deep sleep period or the
[1:12:54] Speaker 1: slow wage sleep, the deep sleep, when you're sort of
[1:12:56] Speaker 1: basically paralyzed. Yeah, you know, you're not moving, you know
[1:12:59] Speaker 1: nothing's going on. Posted when you have your sleep during
[1:13:02] Speaker 1: that period, something opens up in your brain and sends
[1:13:08] Speaker 1: something out there to flush it. And unless you get
[1:13:10] Speaker 1: into that state you don't flush out your brain. Is
[1:13:14] Speaker 1: there a general rule as to how many hours per
[1:13:17] Speaker 1: night or how much of it as a total percentage
[1:13:20] Speaker 1: of your total sleep you should be getting.
[1:13:21] Speaker 2: So a rough sleep hours is slight cycle is about
[1:13:24] Speaker 2: three hours to two of those, so about six hours
[1:13:27] Speaker 2: and probably maybe some break in between. So in and
[1:13:30] Speaker 2: around six hours is the perfect. But obviously we're talking
[1:13:34] Speaker 2: about adults. The younger you are, the more you need,
[1:13:36] Speaker 2: and you know children need more eight ten, et cetera.
[1:13:39] Speaker 2: So I think part of it is to try and
[1:13:42] Speaker 2: ensure that people are used to looking after themselves, to
[1:13:47] Speaker 2: go to sleep, to sleep hygiene.
[1:13:50] Speaker 1: Yeah, it's just so easily. Yeah, and whilst you're leaping too.
[1:13:53] Speaker 2: Yeah, and that's why again exercise, making sure you get
[1:13:55] Speaker 2: a bed when you're fatigued. No booze, no booze, don't
[1:13:58] Speaker 2: drink you know, teaen coffe just before beforehand.
[1:14:01] Speaker 1: You know, try to stay on down, keep your excitement
[1:14:04] Speaker 1: levels down.
[1:14:04] Speaker 2: I think you should write a book on all of this,
[1:14:06] Speaker 2: because you've got all of the keys.
[1:14:07] Speaker 1: Can I can I just ask you one more question?
[1:14:10] Speaker 1: Hopefully it's a comment on a lot of people, on
[1:14:14] Speaker 1: a lot of guys I know older more, my age more,
[1:14:18] Speaker 1: my age category. For many many years have been taking
[1:14:21] Speaker 1: enormous and all sorts of those old school of sleeping tablets.
[1:14:27] Speaker 1: And some people I know, and one of them are,
[1:14:33] Speaker 1: are quite aware and alert when they're sleeping, so they
[1:14:36] Speaker 1: don't get into the deep sleep for as long as
[1:14:39] Speaker 1: other people do because maybe because they're listening, or they're
[1:14:42] Speaker 1: not listening, but sort of instinctively they're listening that any
[1:14:45] Speaker 1: little norms wake, come up, any movement, awakem up. They're aware,
[1:14:49] Speaker 1: but they're asleep sort of thing. And I'm one of
[1:14:51] Speaker 1: those people, and recently I come across these sleeping tables.
[1:14:57] Speaker 1: They're not sleeping tablets, the tubblets which actually blocked the
[1:15:01] Speaker 1: receptors for arecsen in your brain. And I just wonder
[1:15:07] Speaker 1: if there's you might wouldn't get to make comment on
[1:15:11] Speaker 1: it enough as area you even looked at. But rection's
[1:15:14] Speaker 1: the mullog and ee brain there sort of just for
[1:15:17] Speaker 1: the audience that keeps us sort of aware and awakes
[1:15:20] Speaker 1: sort of awaking. It's normal. Seemed tables sort of sedate you,
[1:15:24] Speaker 1: they said, your whole brain, and you basically feel like
[1:15:26] Speaker 1: shit when you wake up because you didn't really sleep.
[1:15:28] Speaker 1: They knocked you out. Whereas these things blocked the receptors
[1:15:32] Speaker 1: on you on your brain cells that actually look grab
[1:15:36] Speaker 1: this RECs and stuff that keep that actually trying to
[1:15:39] Speaker 1: keep you awake, So it sort of blocks that that process.
[1:15:42] Speaker 1: What do you think about those sorts of tablets and
[1:15:45] Speaker 1: you have you have you had much experience with it?
[1:15:48] Speaker 2: Well, what I would say is, again we're talking about
[1:15:50] Speaker 2: upstream and downstream and lots of other things that happened. So,
[1:15:52] Speaker 2: like we've been very interested in erecs and producing cells
[1:15:56] Speaker 2: in the hippocampus because they also control our eating behavior
[1:16:01] Speaker 2: and they're affected in front of temporal dementia and modeor
[1:16:04] Speaker 2: neurine disease. The work that's been done here in Sydney,
[1:16:06] Speaker 2: particularly Rebecca are Mad to show on that those cells
[1:16:10] Speaker 2: are affected early in front of temporal dementia and modeor
[1:16:13] Speaker 2: neurine disease. So although you've taken the approach from the
[1:16:17] Speaker 2: erecs and to sleep, it's also important for your eating
[1:16:20] Speaker 2: behavior and.
[1:16:21] Speaker 1: To have to control the amount of recent or yeah, yeah,
[1:16:25] Speaker 1: that's interesting.
[1:16:25] Speaker 2: Yeah, and they can degenerate and when they degenerate, that's
[1:16:29] Speaker 2: why people start having altered eating behavior. So there's a
[1:16:32] Speaker 2: propensity with certain dementias to like sweet foods, and you know,
[1:16:38] Speaker 2: to eat chocolates, and patients typically become put on weight
[1:16:43] Speaker 2: and become a beast, and to exercise, and that's markers
[1:16:46] Speaker 2: that this could be fronto temporal dementias. What I'm saying
[1:16:48] Speaker 2: is you focus on erection for sleep, but those erections
[1:16:51] Speaker 2: and cells also have other functions. So that's why I'd
[1:16:53] Speaker 2: be always careful in doing thing that might alter function
[1:16:57] Speaker 2: of cells in the brain.
[1:16:58] Speaker 1: Because erection is from the gregwood or rexy, which means
[1:17:01] Speaker 1: we say, when we're saying to someone in Greek, it's
[1:17:07] Speaker 1: a calix, which means good appetite. And it's funny. So
[1:17:12] Speaker 1: now I know why it was fascinating. Now I know
[1:17:14] Speaker 1: why they call it a recitent has something to do
[1:17:17] Speaker 1: with your appetite, it does and eating behavior. Oh right, yeah,
[1:17:21] Speaker 1: So would you expect then if you know, let's say
[1:17:25] Speaker 1: the half life of rex and pill was twenty four hours,
[1:17:28] Speaker 1: for I say it's probably not the case, but that
[1:17:32] Speaker 1: you might lose your hunger, I would say, so, yeah.
[1:17:35] Speaker 1: And the other thing is, though I presume that it
[1:17:37] Speaker 1: bounces back, because it does have a bounce. There's a
[1:17:40] Speaker 1: mad bounce because I've measured it. Uh huh, so I measured.
[1:17:43] Speaker 1: I measured a heart rate and HIV. So and I've
[1:17:48] Speaker 1: watched it go through my So I look at my
[1:17:51] Speaker 1: I go through and I look at my my movements
[1:17:55] Speaker 1: of my heart, my art movements. Because it records everything,
[1:17:58] Speaker 1: and you sleep deep in the beginning, but there's a
[1:18:01] Speaker 1: bounce because the half life actually is five hours. So
[1:18:04] Speaker 1: right towards the end of the sleep period, yeah, your
[1:18:08] Speaker 1: heart rate shoots up big time and your HIV drops
[1:18:11] Speaker 1: big time. Yeah.
[1:18:12] Speaker 2: Yeah, well it's right at the core of functions in
[1:18:15] Speaker 2: the hypothalamus and then.
[1:18:17] Speaker 1: You actually wake up really bright. So to some extent,
[1:18:21] Speaker 1: it's a bit of a trap because you think this
[1:18:23] Speaker 1: is a sleeping tablet. And when I take the Sleepma tableau,
[1:18:26] Speaker 1: wake up and feel really good. I feel really awake,
[1:18:28] Speaker 1: Whereas if I take enormous and normal that the usual
[1:18:32] Speaker 1: types of sleeping tablets, I wake up and feel like
[1:18:34] Speaker 1: shit so immediately that my brain says me, well that's better,
[1:18:38] Speaker 1: that's good. But the reason is is because my recxs
[1:18:41] Speaker 1: and bounce is back the other direction, and I'm actually
[1:18:43] Speaker 1: wide awake and I can actually get away less sleep
[1:18:47] Speaker 1: and feel quite away. But it's just a bounce because
[1:18:50] Speaker 1: all of a sudden you the receptors are now released
[1:18:54] Speaker 1: from they're not blocked, and they grab and everything.
[1:18:57] Speaker 2: What's fascinating. So I presume the ancient Greek must have
[1:19:00] Speaker 2: known a bit about this.
[1:19:01] Speaker 1: They probably did this. Ancient Greek does well. I really
[1:19:07] Speaker 1: enjoyed today. I'm got to ask you this one question
[1:19:09] Speaker 1: from my friend.
[1:19:09] Speaker 2: If you don't monoclonal antibodies, that's what this is.
[1:19:13] Speaker 1: Right.
[1:19:14] Speaker 2: So monoclonal antibodies are now approved in Australia l kenomabed
[1:19:19] Speaker 2: and aanamab, and they're very effective at stripping amyloid from
[1:19:23] Speaker 2: the brain. And we know that so when we do
[1:19:26] Speaker 2: a PET scan, if we do an amyloid PET scan
[1:19:28] Speaker 2: before and after, we can see that the amyloid is
[1:19:30] Speaker 2: either cleared or that the volume is right.
[1:19:34] Speaker 1: Down post taking the monoclonal. Yeah, anybody.
[1:19:39] Speaker 2: But then you may say to me, Okay, that's the case,
[1:19:42] Speaker 2: and that protein is the critical driver of Alzheimer's disease.
[1:19:46] Speaker 2: The patient should be completely back to normal, but they're
[1:19:48] Speaker 2: not so, and that's where research is at. So we're
[1:19:52] Speaker 2: clearing amyloid, but the patients aren't necessarily getting better, But
[1:19:56] Speaker 2: what's happening is you're slow in the decline. You're turning
[1:19:59] Speaker 2: the disease process back perps up to three years, right, okay,
[1:20:04] Speaker 2: but cutting edge eries and these are patients who have
[1:20:06] Speaker 2: had already manifestations and memory problems, but they're not too
[1:20:11] Speaker 2: far affected because it's too late, so they have to
[1:20:14] Speaker 2: have a mild effect in their brain function. But the
[1:20:18] Speaker 2: cutting edge then is what if we treated people, you know,
[1:20:22] Speaker 2: before they developed the condition. So we're looking at now,
[1:20:24] Speaker 2: this is research that's being underway at at Neuroscience Research
[1:20:28] Speaker 2: Australia and Emma Devenue I think he spoke to as
[1:20:30] Speaker 2: one of the key drivers of that. So she's she's
[1:20:33] Speaker 2: treating patients who have genetic malformations linked to Alzheimer's disease
[1:20:38] Speaker 2: with these monoclonal antibodies in the hope they'll never develop
[1:20:41] Speaker 2: the condition. And already we're seeing that if the families
[1:20:44] Speaker 2: were developing, say Alzheimer's disease at forty five point fifty,
[1:20:48] Speaker 2: they're passing those ages without developing the condition. Oh wow, yeah,
[1:20:51] Speaker 2: so it's having an effect. But also these are early
[1:20:54] Speaker 2: generation therapies. In other words, that's the first type of approach,
[1:20:58] Speaker 2: there'd be more ederations, and there's so many coming through
[1:21:03] Speaker 2: right now as we speak.
[1:21:04] Speaker 1: So one of those two monoclinal antibodies called it's.
[1:21:07] Speaker 2: A nanomab and look Canama, there may be means monoclonal
[1:21:11] Speaker 2: antibodies and they're two different companies.
[1:21:13] Speaker 1: And they're both are both basically available through neurologies. If
[1:21:16] Speaker 1: you're a person in this category.
[1:21:17] Speaker 2: There are people being treated here in Sydney now, so
[1:21:20] Speaker 2: it's approved by the TGA. It hasn't yet been approved
[1:21:23] Speaker 2: by the Pharmaceutical Benefits Advisory Committee, so you get paid
[1:21:26] Speaker 2: for it. So yeah, so standard and don't quote me
[1:21:30] Speaker 2: on this, but a standard treatment course would be about
[1:21:33] Speaker 2: one hundred thousand dollars. But if you if you want
[1:21:36] Speaker 2: to preserve your brain function, it's worth it. It's absolutely
[1:21:38] Speaker 2: if you afford it, absolutely worth it if you can
[1:21:41] Speaker 2: tap into your super and use it.
[1:21:43] Speaker 1: And I had one final question for you, just in
[1:21:46] Speaker 1: terms of and if I could just go back to
[1:21:49] Speaker 1: cholesterol and to these stads, that that's a problem for
[1:21:52] Speaker 1: your brain too. And let's say you're and I'd like
[1:21:57] Speaker 1: you to comment on this. Let's say yours statin you're
[1:22:01] Speaker 1: not able to take saturns. You know, for some reason
[1:22:04] Speaker 1: the statins affecture sleep, but whatever the case may be,
[1:22:08] Speaker 1: and sleeps critical. So there are now injections you can
[1:22:13] Speaker 1: get which actually don't cross the blood brain barrier and
[1:22:19] Speaker 1: lake statins do, and it will reduce significantly reduce your LDAL.
[1:22:27] Speaker 1: Would you just like to comment on.
[1:22:28] Speaker 2: That, Well, we're just talking about monoclonal antibodies. So monoclinal
[1:22:32] Speaker 2: antibodies actually came from hematology for cancers. They're very effective
[1:22:36] Speaker 2: in melanoma. We're now putting them into the brain for
[1:22:39] Speaker 2: Alzheimer's disease. They're also very very effective for cholesterol control.
[1:22:43] Speaker 2: So monoclonal antibodies are available for lowering cholesterol. But obviously
[1:22:49] Speaker 2: that needs to be under pharmaceutical benefit scheme. There are
[1:22:52] Speaker 2: certain people who are entitled to it, are not, and
[1:22:54] Speaker 2: there are markers. It's not really my area, but there
[1:22:58] Speaker 2: are people who focus on. But if it works, it
[1:23:01] Speaker 2: does work. It's very effective.
[1:23:02] Speaker 1: And if it's effective, if you can get your cholesterol
[1:23:05] Speaker 1: down to the levels where it's like in the right territory, yeah,
[1:23:09] Speaker 1: then it's good for your brain.
[1:23:10] Speaker 2: It's fantastic for the brain. And again that's going to
[1:23:13] Speaker 2: be transformational for our community. That's that's that's an amazing development.
[1:23:17] Speaker 1: You know, I'm about to try it, but I'm not
[1:23:20] Speaker 1: someone to qualifies under the pharmaceutical benefit scheme. I paid
[1:23:24] Speaker 1: for it. Yeah, it's not cheap, but you have to
[1:23:26] Speaker 1: go I think two injections a year, and you do
[1:23:28] Speaker 1: one where you just do it every week or whatever is.
[1:23:30] Speaker 1: But there's another one. We get two injections a year,
[1:23:32] Speaker 1: but allegedly at Regicial audio by fifty percent.
[1:23:36] Speaker 2: Quite quickly, incredibly effective.
[1:23:38] Speaker 1: Yeah, it activates more receptors to grab hold of more
[1:23:40] Speaker 1: older right, because there's something in your that turns out
[1:23:45] Speaker 1: that blocks these receptors. What they do is they stop that.
[1:23:49] Speaker 1: I think it's PCSK or nineteen is the name of
[1:23:53] Speaker 1: the you know, the molecule, and that turns it stops that.
[1:23:57] Speaker 1: It turns that off and then your receptors are grabbing
[1:23:59] Speaker 1: all the elder that can on yourselves and that and
[1:24:03] Speaker 1: that's this ingestion just fixes that part, so it goes
[1:24:06] Speaker 1: nowhere else just go straight there and sorts it out.
[1:24:08] Speaker 1: It's pretty amazing and great science. And again some scientists
[1:24:12] Speaker 1: has worked this stuff out. They probably were doing it
[1:24:14] Speaker 1: with something using it for something else at some stage,
[1:24:17] Speaker 1: and all these things, as you say, you always say,
[1:24:20] Speaker 1: and I want everyone to remember this, that what's good
[1:24:22] Speaker 1: for your heart is good for your brain. Fantastic going
[1:24:26] Speaker 1: to that, Matthew. Thanks very much, Thanks.
[1:24:28] Speaker 2: Mark, and and thanks for your support for brain health,
[1:24:31] Speaker 2: mental health and and also for neuroscience research Australia. We're
[1:24:34] Speaker 2: really grateful, so thank you for most of them.

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